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human cthrc1 protein  (MedChemExpress)
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MedChemExpress human cthrc1 protein
(A) A and B: bulk RNA-seq of aortic tissues from control and AD mice (n=3 per group). Volcano plot displaying differentially expressed genes in aortas between the two groups. <t>Cthrc1</t> was significantly up-regulated in AD mouse models. (B) KEGG enrichment analysis of differentially expressed genes in aortic tissues from control and AD mice. (C) C to F: scRNA-seq data of 4 samples from control and AD mice. Violin plots showing nFeature, nCount, percent.mt and expression level of the housekeeping gene beta-actin (Actb) after quality control of 4 samples. (D) UMAP plot of 82,326 single cells from 4 samples colored according to the 15 clusters. (E) Heatmap showing expression signatures of the marker genes in each cell type. (F) Heatmap showing expression signatures of the top differentially expressed genes in 2 fibroblast subclusters. (G) UMAP plots showing CTHRC1 expression in fibroblasts from control individuals and patients with ascending thoracic aortic aneurysm (GSE155468). (H) H to J: CTHRC1 protein levels in vitro (NIH3T3 cells (H), human umbilical vein endothelial cells (HUVECs) (I), and MOVAS cells(J), incubated with Ang-II (10^-6 M) and BAPN (0.2 mM). (K) bulk RNA sequencing of aortas in male and female mice. PCA of gene profiles of transcriptome between different sexes. (L) Volcano plot displaying differentially expressed genes in aortic tissues from control and AD female mice (n=3 per group). Cthrc1 was also significantly up-regulated in AD female mouse models. (M) KEGG enrichment analysis of the differentially expressed genes in AD female mouse models. (N) Immunohistochemical staining for CTHRC1 in female mouse aortas. The orange arrows indicate CTHRC1 expression in adventitial fibroblasts of the dissected aortas. (O) Female mouse serum CTHRC1 content in control and AD mice (n=6). (an unpaired two-tailed Student’s t-test, **** P ≤ 0.0001.)
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(A) A and B: bulk RNA-seq of aortic tissues from control and AD mice (n=3 per group). Volcano plot displaying differentially expressed genes in aortas between the two groups. Cthrc1 was significantly up-regulated in AD mouse models. (B) KEGG enrichment analysis of differentially expressed genes in aortic tissues from control and AD mice. (C) C to F: scRNA-seq data of 4 samples from control and AD mice. Violin plots showing nFeature, nCount, percent.mt and expression level of the housekeeping gene beta-actin (Actb) after quality control of 4 samples. (D) UMAP plot of 82,326 single cells from 4 samples colored according to the 15 clusters. (E) Heatmap showing expression signatures of the marker genes in each cell type. (F) Heatmap showing expression signatures of the top differentially expressed genes in 2 fibroblast subclusters. (G) UMAP plots showing CTHRC1 expression in fibroblasts from control individuals and patients with ascending thoracic aortic aneurysm (GSE155468). (H) H to J: CTHRC1 protein levels in vitro (NIH3T3 cells (H), human umbilical vein endothelial cells (HUVECs) (I), and MOVAS cells(J), incubated with Ang-II (10^-6 M) and BAPN (0.2 mM). (K) bulk RNA sequencing of aortas in male and female mice. PCA of gene profiles of transcriptome between different sexes. (L) Volcano plot displaying differentially expressed genes in aortic tissues from control and AD female mice (n=3 per group). Cthrc1 was also significantly up-regulated in AD female mouse models. (M) KEGG enrichment analysis of the differentially expressed genes in AD female mouse models. (N) Immunohistochemical staining for CTHRC1 in female mouse aortas. The orange arrows indicate CTHRC1 expression in adventitial fibroblasts of the dissected aortas. (O) Female mouse serum CTHRC1 content in control and AD mice (n=6). (an unpaired two-tailed Student’s t-test, **** P ≤ 0.0001.)

Journal: bioRxiv

Article Title: CTHRC1 is a new therapeutic target and serum diagnostic biomarker for aortic dissection

doi: 10.1101/2025.04.19.649636

Figure Lengend Snippet: (A) A and B: bulk RNA-seq of aortic tissues from control and AD mice (n=3 per group). Volcano plot displaying differentially expressed genes in aortas between the two groups. Cthrc1 was significantly up-regulated in AD mouse models. (B) KEGG enrichment analysis of differentially expressed genes in aortic tissues from control and AD mice. (C) C to F: scRNA-seq data of 4 samples from control and AD mice. Violin plots showing nFeature, nCount, percent.mt and expression level of the housekeeping gene beta-actin (Actb) after quality control of 4 samples. (D) UMAP plot of 82,326 single cells from 4 samples colored according to the 15 clusters. (E) Heatmap showing expression signatures of the marker genes in each cell type. (F) Heatmap showing expression signatures of the top differentially expressed genes in 2 fibroblast subclusters. (G) UMAP plots showing CTHRC1 expression in fibroblasts from control individuals and patients with ascending thoracic aortic aneurysm (GSE155468). (H) H to J: CTHRC1 protein levels in vitro (NIH3T3 cells (H), human umbilical vein endothelial cells (HUVECs) (I), and MOVAS cells(J), incubated with Ang-II (10^-6 M) and BAPN (0.2 mM). (K) bulk RNA sequencing of aortas in male and female mice. PCA of gene profiles of transcriptome between different sexes. (L) Volcano plot displaying differentially expressed genes in aortic tissues from control and AD female mice (n=3 per group). Cthrc1 was also significantly up-regulated in AD female mouse models. (M) KEGG enrichment analysis of the differentially expressed genes in AD female mouse models. (N) Immunohistochemical staining for CTHRC1 in female mouse aortas. The orange arrows indicate CTHRC1 expression in adventitial fibroblasts of the dissected aortas. (O) Female mouse serum CTHRC1 content in control and AD mice (n=6). (an unpaired two-tailed Student’s t-test, **** P ≤ 0.0001.)

Article Snippet: And confluent MOVAS and HASMCs (80%–90%) were treated with recombinant human CTHRC1 Protein (1ug/mL) (HY-P70092, MedChemExpress) to investigate its effect on vascular remodeling in vitro.

Techniques: RNA Sequencing, Control, Expressing, Marker, In Vitro, Incubation, Immunohistochemical staining, Staining, Two Tailed Test

(A) A schematic diagram illustrating the experiment design. Single-cell RNA sequencing was applied to 4 samples from C57BL/6 mice that were infused with saline or simultaneously administrated by Ang-II/BAPN for 14 days. (B) UMAP plot of the 82,326 single cells from the 4 samples outlined in (A), showing the identification of 9 main clusters. (C) The proportion of 9 cell clusters in control and AD mice. (D) UMAP plot of the 9,043 fibroblasts with 2 subclusters. (E) UMAP plots showing comparison of fibroblast clusters or Cthrc1 expression between the AD and control group. (F) Immunohistochemical staining for CTHRC1 in mouse aortas. The orange arrows indicating CTHRC1 expression in adventitial fibroblasts of the dissected aortas. (G) Representative images showing immunoblotting analysis of CTHRC1 levels in control and AD mice (n=6). (H) Mouse serum CTHRC1 content in control and AD groups (n=6). Data are presented as mean ± SEM. (Student’s t test, ** P ≤ 0.01.) (I) Heatmap of expression levels of genes related to vascular smooth muscle cell contraction and extracellular matrix disassembly between control and AD mice. (J) Scatterplot showing gene expression level in the adventitia between A+ Pos and A+ Neg samples. Red: upregulated genes in the adventitia of aortas from patients prone to aorta rupture, blue: downregulated genes. See also .

Journal: bioRxiv

Article Title: CTHRC1 is a new therapeutic target and serum diagnostic biomarker for aortic dissection

doi: 10.1101/2025.04.19.649636

Figure Lengend Snippet: (A) A schematic diagram illustrating the experiment design. Single-cell RNA sequencing was applied to 4 samples from C57BL/6 mice that were infused with saline or simultaneously administrated by Ang-II/BAPN for 14 days. (B) UMAP plot of the 82,326 single cells from the 4 samples outlined in (A), showing the identification of 9 main clusters. (C) The proportion of 9 cell clusters in control and AD mice. (D) UMAP plot of the 9,043 fibroblasts with 2 subclusters. (E) UMAP plots showing comparison of fibroblast clusters or Cthrc1 expression between the AD and control group. (F) Immunohistochemical staining for CTHRC1 in mouse aortas. The orange arrows indicating CTHRC1 expression in adventitial fibroblasts of the dissected aortas. (G) Representative images showing immunoblotting analysis of CTHRC1 levels in control and AD mice (n=6). (H) Mouse serum CTHRC1 content in control and AD groups (n=6). Data are presented as mean ± SEM. (Student’s t test, ** P ≤ 0.01.) (I) Heatmap of expression levels of genes related to vascular smooth muscle cell contraction and extracellular matrix disassembly between control and AD mice. (J) Scatterplot showing gene expression level in the adventitia between A+ Pos and A+ Neg samples. Red: upregulated genes in the adventitia of aortas from patients prone to aorta rupture, blue: downregulated genes. See also .

Article Snippet: And confluent MOVAS and HASMCs (80%–90%) were treated with recombinant human CTHRC1 Protein (1ug/mL) (HY-P70092, MedChemExpress) to investigate its effect on vascular remodeling in vitro.

Techniques: RNA Sequencing, Saline, Control, Comparison, Expressing, Immunohistochemical staining, Staining, Western Blot, Gene Expression

(A) Experiment design. 6-week-old male Cthrc1 -/- mice (n=16) and wide type (WT) mice (n=18) were treated with saline or Ang-II/BAPN for 14 days. (B) Representative images of immunoblotting analysis of CTHRC1 levels in aortas from the mice in A. Bottom: quantification of CTHRC1 expression in aortas. (a ordinary one-way ANOVA followed by Bonferroni’s multiple comparison test, ** P ≤ 0.01.) (C) Representative ultrasound images of aorta in mice (scale bar, 1mm). (D) Measurements of maximum aortic diameter of mice in A (n=6-9 per group). (a ordinary one-way ANOVA followed by Bonferroni’s multiple comparison test, ** P ≤ 0.01, *** P ≤ 0.0001.) (E) Representative pictures of whole aortas from the mice in A. The yellow arrows indicate the dissected sites of vascular lesions. (F) Quantification of AD incidence in the whole aorta, ascending, thoracic and abdominal aortas from WT and Cthrc1 -/- mice. (Fisher’s exact test, * P ≤ 0.05.) (G) Kaplan-Meier survival rates analysis of the mice in A. (Kaplan-Meier survival rates analysis, * P ≤ 0.05, ns, no significance.) (H) Representative images of histological staining with hematoxylin and eosin in aortic sections from the mice in A. Right: measurements of aortic wall thickness of aortas (scale bar, 50 μm). (a ordinary one-way ANOVA followed by Bonferroni’s multiple comparison test, ** P ≤ 0.01.) (I) Representative images of Elastica van Gieson staining in aortic sections from the mice in A. Right: measurement of numbers of elastin breaks per vessel (scale bar, 100 μm). (a ordinary one-way ANOVA followed by Bonferroni’s multiple comparison test, *** P ≤ 0.0001). (J) UMAP plot of the 28,700 single cells from WT and Cthrc1 -/- mice challenged with Ang-II/BAPN for 14 days, displaying the identification of 8 major clusters. (K) The proportion of 8 cell clusters in WT and Cthrc1 -/- mice infused with Ang-II/BAPN. (L) Upper: UMAP plot of fibroblast subclusters in the WT group and Cthrc1 -/- group respectively. Bottom: the proportion of FB1 and FB2. (M) KEGG enrichment analysis of differentially expressed genes in aortic tissues from WT and Cthrc1 -/- mice analyzed by bulk-RNA seq data. (N) Heatmap showing the expression levels of genes related to vascular smooth muscle cell contraction and extracellular matrix disassembly. See also .

Journal: bioRxiv

Article Title: CTHRC1 is a new therapeutic target and serum diagnostic biomarker for aortic dissection

doi: 10.1101/2025.04.19.649636

Figure Lengend Snippet: (A) Experiment design. 6-week-old male Cthrc1 -/- mice (n=16) and wide type (WT) mice (n=18) were treated with saline or Ang-II/BAPN for 14 days. (B) Representative images of immunoblotting analysis of CTHRC1 levels in aortas from the mice in A. Bottom: quantification of CTHRC1 expression in aortas. (a ordinary one-way ANOVA followed by Bonferroni’s multiple comparison test, ** P ≤ 0.01.) (C) Representative ultrasound images of aorta in mice (scale bar, 1mm). (D) Measurements of maximum aortic diameter of mice in A (n=6-9 per group). (a ordinary one-way ANOVA followed by Bonferroni’s multiple comparison test, ** P ≤ 0.01, *** P ≤ 0.0001.) (E) Representative pictures of whole aortas from the mice in A. The yellow arrows indicate the dissected sites of vascular lesions. (F) Quantification of AD incidence in the whole aorta, ascending, thoracic and abdominal aortas from WT and Cthrc1 -/- mice. (Fisher’s exact test, * P ≤ 0.05.) (G) Kaplan-Meier survival rates analysis of the mice in A. (Kaplan-Meier survival rates analysis, * P ≤ 0.05, ns, no significance.) (H) Representative images of histological staining with hematoxylin and eosin in aortic sections from the mice in A. Right: measurements of aortic wall thickness of aortas (scale bar, 50 μm). (a ordinary one-way ANOVA followed by Bonferroni’s multiple comparison test, ** P ≤ 0.01.) (I) Representative images of Elastica van Gieson staining in aortic sections from the mice in A. Right: measurement of numbers of elastin breaks per vessel (scale bar, 100 μm). (a ordinary one-way ANOVA followed by Bonferroni’s multiple comparison test, *** P ≤ 0.0001). (J) UMAP plot of the 28,700 single cells from WT and Cthrc1 -/- mice challenged with Ang-II/BAPN for 14 days, displaying the identification of 8 major clusters. (K) The proportion of 8 cell clusters in WT and Cthrc1 -/- mice infused with Ang-II/BAPN. (L) Upper: UMAP plot of fibroblast subclusters in the WT group and Cthrc1 -/- group respectively. Bottom: the proportion of FB1 and FB2. (M) KEGG enrichment analysis of differentially expressed genes in aortic tissues from WT and Cthrc1 -/- mice analyzed by bulk-RNA seq data. (N) Heatmap showing the expression levels of genes related to vascular smooth muscle cell contraction and extracellular matrix disassembly. See also .

Article Snippet: And confluent MOVAS and HASMCs (80%–90%) were treated with recombinant human CTHRC1 Protein (1ug/mL) (HY-P70092, MedChemExpress) to investigate its effect on vascular remodeling in vitro.

Techniques: Saline, Western Blot, Expressing, Comparison, Staining, RNA Sequencing

(A) Immunohistochemical staining for CTHRC1 in aortas from the Cthrc1 -/- and WT mice. The orange arrows indicate CTHRC1 expression in adventitial fibroblasts of the dissected aortas, with no positive staining observed in Cthrc1 -/- group. (B) Alican blue staining of aortas from the Cthrc1 -/- and WT mice. (C) C to F: bulk RNA-seq of aortic tissues from WT and Cthrc1 -/- mice. GSEA showing the inhibition of extracellular matrix disassembly and the activation of vascular smooth muscle contraction. (D) : D to F: Violin plots illustrating gene expressions of MMPs (D), ADAMs (E) and ADAMTSs (F) between WT and Cthrc1 -/- mice infused with Ang-II/BAPN. MMPs: matrix metalloproteinases; ADAMs: a disintegrin and metalloproteinases; ADAMTSs: ADAMs with a thrombospondin motif. (G) G to P: 6-week-old female Cthrc1 -/- mice (n=16) and WT mice (n=18) were treated with saline or Ang-II/BAPN for 14 days. Representative ultrasound images of aorta in female mice (scale bar, 1mm). (H) Measurements of maximum aortic diameter of mice in G (n=8 per group). (a Welch ANOVA test followed by a post hoc analysis using the Tamhane T2 method, *** P ≤ 0.001; ** P ≤ 0.01.) (I) Representative pictures of whole aortas from the female mice. The yellow arrows indicate the dissected sites of vascular lesions. (J) Quantification of AD incidence in the whole aorta, ascending, thoracic and abdominal aortas from WT and Cthrc1 -/- female mice. (Fisher’s exact test, * P ≤ 0.05.) (K) Kaplan-Meier survival rates analysis of the four groups of female mice. (Kaplan-Meier survival rates analysis, ns, no significance.) (L) Immunohistochemical staining for CTHRC1 in aortas from the female mice. The orange arrows indicate CTHRC1 expression in adventitial fibroblasts of the dissected aortas from the WT female mice, with no positive staining observed in Cthrc1 -/- female mice (scale bar, 50 μm). (M) Representative images of histological staining with hematoxylin and eosin in aortic sections from the female mice (scale bar, 50 μm). (N) Measurements of aortic wall thickness of aortas. (a ordinary one-way ANOVA followed by Bonferroni’s multiple comparison test, *** P ≤ 0.001; **** P ≤ 0.0001.) (O) Representative images of EVG staining in aortic sections from the female mice (scale bar, 50 μm). (P) Measurements of numbers of elastin breaks per vessel. (a ordinary one-way ANOVA followed by Bonferroni’s multiple comparison test, ** P ≤ 0.01; *** P ≤ 0.001.) (Q) Q to S: bulk RNA-seq of aortic tissues from WT and Cthrc1 -/- female mice. PCA of gene profiles of transcriptome between different sexes. (R) KEGG enrichment analysis of differentially expressed genes in aortic tissues from WT and Cthrc1 -/- female mice. (S) Heatmap showing the expression levels of genes related to vascular smooth muscle cell contraction.

Journal: bioRxiv

Article Title: CTHRC1 is a new therapeutic target and serum diagnostic biomarker for aortic dissection

doi: 10.1101/2025.04.19.649636

Figure Lengend Snippet: (A) Immunohistochemical staining for CTHRC1 in aortas from the Cthrc1 -/- and WT mice. The orange arrows indicate CTHRC1 expression in adventitial fibroblasts of the dissected aortas, with no positive staining observed in Cthrc1 -/- group. (B) Alican blue staining of aortas from the Cthrc1 -/- and WT mice. (C) C to F: bulk RNA-seq of aortic tissues from WT and Cthrc1 -/- mice. GSEA showing the inhibition of extracellular matrix disassembly and the activation of vascular smooth muscle contraction. (D) : D to F: Violin plots illustrating gene expressions of MMPs (D), ADAMs (E) and ADAMTSs (F) between WT and Cthrc1 -/- mice infused with Ang-II/BAPN. MMPs: matrix metalloproteinases; ADAMs: a disintegrin and metalloproteinases; ADAMTSs: ADAMs with a thrombospondin motif. (G) G to P: 6-week-old female Cthrc1 -/- mice (n=16) and WT mice (n=18) were treated with saline or Ang-II/BAPN for 14 days. Representative ultrasound images of aorta in female mice (scale bar, 1mm). (H) Measurements of maximum aortic diameter of mice in G (n=8 per group). (a Welch ANOVA test followed by a post hoc analysis using the Tamhane T2 method, *** P ≤ 0.001; ** P ≤ 0.01.) (I) Representative pictures of whole aortas from the female mice. The yellow arrows indicate the dissected sites of vascular lesions. (J) Quantification of AD incidence in the whole aorta, ascending, thoracic and abdominal aortas from WT and Cthrc1 -/- female mice. (Fisher’s exact test, * P ≤ 0.05.) (K) Kaplan-Meier survival rates analysis of the four groups of female mice. (Kaplan-Meier survival rates analysis, ns, no significance.) (L) Immunohistochemical staining for CTHRC1 in aortas from the female mice. The orange arrows indicate CTHRC1 expression in adventitial fibroblasts of the dissected aortas from the WT female mice, with no positive staining observed in Cthrc1 -/- female mice (scale bar, 50 μm). (M) Representative images of histological staining with hematoxylin and eosin in aortic sections from the female mice (scale bar, 50 μm). (N) Measurements of aortic wall thickness of aortas. (a ordinary one-way ANOVA followed by Bonferroni’s multiple comparison test, *** P ≤ 0.001; **** P ≤ 0.0001.) (O) Representative images of EVG staining in aortic sections from the female mice (scale bar, 50 μm). (P) Measurements of numbers of elastin breaks per vessel. (a ordinary one-way ANOVA followed by Bonferroni’s multiple comparison test, ** P ≤ 0.01; *** P ≤ 0.001.) (Q) Q to S: bulk RNA-seq of aortic tissues from WT and Cthrc1 -/- female mice. PCA of gene profiles of transcriptome between different sexes. (R) KEGG enrichment analysis of differentially expressed genes in aortic tissues from WT and Cthrc1 -/- female mice. (S) Heatmap showing the expression levels of genes related to vascular smooth muscle cell contraction.

Article Snippet: And confluent MOVAS and HASMCs (80%–90%) were treated with recombinant human CTHRC1 Protein (1ug/mL) (HY-P70092, MedChemExpress) to investigate its effect on vascular remodeling in vitro.

Techniques: Immunohistochemical staining, Staining, Expressing, RNA Sequencing, Inhibition, Activation Assay, Saline, Comparison

(A) Comparison of the total number of cell-cell interactions and the interaction strength from the scRNA-seq data of control and AD mice. (B) Circle plot showing differential cell-cell interaction numbers and strength between fibroblast, SMC, EC, MoMaphDC, Schwann, B cell and T cell clusters predicted by CellChat. Each circle represents one cell cluster, edges between circles represent intercellular signaling between cell clusters, and edge thickness reflects interaction number or strength. Red edges represent increased interaction number or strength and blue represent decreased interaction number or strength in AD mice versus control mice. (C) Identification of up-regulated signaling by comparing the communication probabilities mediated by ligand–receptor pairs from fibroblasts to SMCs in AD mouse models. (D) D to H: scRNA-seq of the two aortas from WT and Cthrc1 -/- mice infused with Ang-II/BAPN for 14 days were pooled per group. The proportion of major cell types including SMCs, ECs and FBs in Ang-II/BAPN-infused WT and Cthrc1 -/- mice. (E) Bar diagram showing the percentage of 4 subclusters in aortic SMCs from the two groups of mice. (F) Boxplot illustrating the differential gene expression of contractile genes in aortic SMCs of the two mouse groups. (* P ≤ 0.05, ** P ≤ 0.01, *** P ≤ 0.0001. ns, no significance.) (G) Barplot depicting the numbers of differential expressed genes in SMC subclusters of the two mouse groups. (H) Gene Ontology enrichment analysis of down-regulated genes in fibromyocytes of the two mouse groups. (I) Immunofluorescence staining of α-SMA and SM22α expression in aortas from Ang-II/BAPN-infused WT and Cthrc1 -/- mice. DAPI: 4’,6-diamidino-2-phenylindole (scale bar: 100 μm). (J) Quantification of α-SMA and SM22α positive area in aortas. (a ordinary one-way ANOVA followed by Bonferroni’s multiple comparison test, **** P ≤ 0.00001.) (K) K to L: Incubating the murine aortic smooth muscle cells (MOVAS) with rhCTHRC1 in vitro. Gene Ontology enrichment analysis of up-regulated genes in MOVAS cells treated with rhCTHRC1 by bulk RNA-seq. (L) Heatmap showing the expression levels of genes related to metallopeptidase activity, activation of MAPKK activity and positive regulation of smooth muscle cell proliferation in MOVAS cells treated with rhCTHRC1 or Vehicle. (M) Immunoblotting analysis of the protein levels of α-SMA, SM22α, and p-ERK1/2 in MOVAS with or without rhCTHRC1 treatment. See also .

Journal: bioRxiv

Article Title: CTHRC1 is a new therapeutic target and serum diagnostic biomarker for aortic dissection

doi: 10.1101/2025.04.19.649636

Figure Lengend Snippet: (A) Comparison of the total number of cell-cell interactions and the interaction strength from the scRNA-seq data of control and AD mice. (B) Circle plot showing differential cell-cell interaction numbers and strength between fibroblast, SMC, EC, MoMaphDC, Schwann, B cell and T cell clusters predicted by CellChat. Each circle represents one cell cluster, edges between circles represent intercellular signaling between cell clusters, and edge thickness reflects interaction number or strength. Red edges represent increased interaction number or strength and blue represent decreased interaction number or strength in AD mice versus control mice. (C) Identification of up-regulated signaling by comparing the communication probabilities mediated by ligand–receptor pairs from fibroblasts to SMCs in AD mouse models. (D) D to H: scRNA-seq of the two aortas from WT and Cthrc1 -/- mice infused with Ang-II/BAPN for 14 days were pooled per group. The proportion of major cell types including SMCs, ECs and FBs in Ang-II/BAPN-infused WT and Cthrc1 -/- mice. (E) Bar diagram showing the percentage of 4 subclusters in aortic SMCs from the two groups of mice. (F) Boxplot illustrating the differential gene expression of contractile genes in aortic SMCs of the two mouse groups. (* P ≤ 0.05, ** P ≤ 0.01, *** P ≤ 0.0001. ns, no significance.) (G) Barplot depicting the numbers of differential expressed genes in SMC subclusters of the two mouse groups. (H) Gene Ontology enrichment analysis of down-regulated genes in fibromyocytes of the two mouse groups. (I) Immunofluorescence staining of α-SMA and SM22α expression in aortas from Ang-II/BAPN-infused WT and Cthrc1 -/- mice. DAPI: 4’,6-diamidino-2-phenylindole (scale bar: 100 μm). (J) Quantification of α-SMA and SM22α positive area in aortas. (a ordinary one-way ANOVA followed by Bonferroni’s multiple comparison test, **** P ≤ 0.00001.) (K) K to L: Incubating the murine aortic smooth muscle cells (MOVAS) with rhCTHRC1 in vitro. Gene Ontology enrichment analysis of up-regulated genes in MOVAS cells treated with rhCTHRC1 by bulk RNA-seq. (L) Heatmap showing the expression levels of genes related to metallopeptidase activity, activation of MAPKK activity and positive regulation of smooth muscle cell proliferation in MOVAS cells treated with rhCTHRC1 or Vehicle. (M) Immunoblotting analysis of the protein levels of α-SMA, SM22α, and p-ERK1/2 in MOVAS with or without rhCTHRC1 treatment. See also .

Article Snippet: And confluent MOVAS and HASMCs (80%–90%) were treated with recombinant human CTHRC1 Protein (1ug/mL) (HY-P70092, MedChemExpress) to investigate its effect on vascular remodeling in vitro.

Techniques: Comparison, Control, Gene Expression, Immunofluorescence, Staining, Expressing, In Vitro, RNA Sequencing, Activity Assay, Activation Assay, Western Blot

(A) A to G: scRNA-seq data of aortas from WT and Cthrc1 -/- mice challenged with Ang-II/BAPN for 14 days. Violin plots showing data characteristics on nFeature, nCount and percent.mt after quality control of the two groups. (B) The violin plot showing the expression level of the housekeeping gene beta-actin (Actb) between the two groups. The relative stability of Actb expression indicates consistency. (C) UMAP plot of 82,326 single cells from the samples colored according to the 14 clusters. (D) Heatmap showing expression signatures of the marker genes in each cell type. (E) UMAP plot of 1,962 SMCs colored according to the identified 4 SMC subclusters. (F) Heatmap showing the scaled mean expression of signature genes in 4 SMC subclusters. (G) Gene Ontology enrichment analysis of up-regulated genes in contractile SMCs of the two groups of mice. (H) Immunoblotting analysis of α-SMA and SM22α expression in aortas from Ang-II/BAPN-infused WT and Cthrc1 -/- mice (n=6). (I) Quantification of α-SMA and SM22α protein expression levels. (a ordinary one-way ANOVA followed by Bonferroni’s multiple comparison test, *** P ≤ 0.001, **** P ≤ 0.0001.) (J) J and K: whole transcriptome analysis of MOVAS cells treated with vehicle and rhCTHRC1. A volcano plot displaying differentially expressed genes. Upward expression of Dcn , Adam9 , Angpt2 and Mmp8 gene in the presence of rhCTHRC1. (K) KEGG enrichment analysis of up-regulated genes in aortas from Ang-II/BAPN-infused WT and Cthrc1 -/- mice.

Journal: bioRxiv

Article Title: CTHRC1 is a new therapeutic target and serum diagnostic biomarker for aortic dissection

doi: 10.1101/2025.04.19.649636

Figure Lengend Snippet: (A) A to G: scRNA-seq data of aortas from WT and Cthrc1 -/- mice challenged with Ang-II/BAPN for 14 days. Violin plots showing data characteristics on nFeature, nCount and percent.mt after quality control of the two groups. (B) The violin plot showing the expression level of the housekeeping gene beta-actin (Actb) between the two groups. The relative stability of Actb expression indicates consistency. (C) UMAP plot of 82,326 single cells from the samples colored according to the 14 clusters. (D) Heatmap showing expression signatures of the marker genes in each cell type. (E) UMAP plot of 1,962 SMCs colored according to the identified 4 SMC subclusters. (F) Heatmap showing the scaled mean expression of signature genes in 4 SMC subclusters. (G) Gene Ontology enrichment analysis of up-regulated genes in contractile SMCs of the two groups of mice. (H) Immunoblotting analysis of α-SMA and SM22α expression in aortas from Ang-II/BAPN-infused WT and Cthrc1 -/- mice (n=6). (I) Quantification of α-SMA and SM22α protein expression levels. (a ordinary one-way ANOVA followed by Bonferroni’s multiple comparison test, *** P ≤ 0.001, **** P ≤ 0.0001.) (J) J and K: whole transcriptome analysis of MOVAS cells treated with vehicle and rhCTHRC1. A volcano plot displaying differentially expressed genes. Upward expression of Dcn , Adam9 , Angpt2 and Mmp8 gene in the presence of rhCTHRC1. (K) KEGG enrichment analysis of up-regulated genes in aortas from Ang-II/BAPN-infused WT and Cthrc1 -/- mice.

Article Snippet: And confluent MOVAS and HASMCs (80%–90%) were treated with recombinant human CTHRC1 Protein (1ug/mL) (HY-P70092, MedChemExpress) to investigate its effect on vascular remodeling in vitro.

Techniques: Control, Expressing, Marker, Western Blot, Comparison

(A) Workflow of the immunoprecipitation (IP) of CTHRC1 identified by mass spectrometry (MS). (B) Venn diagram of intersection analyses of two independent assays for potential receptors of CTHRC1 on MOVAS cells. Right: Scores of candidate binding proteins identified by MS. (C) Co-IP-blotting of CTHRC1 with ADAM9 receptor on MOVAS cells. (D) D to E: whole transcriptome analysis of MOVAS cells incubated with rhCTHRC1, knockouting Roas26 (control) or Adam9 ( Adam9 -KO). Gene Ontology enrichment analysis of down-regulated genes in Adam9 -KO MOVAS cells treated with rhCTHRC1. (E) Heatmap showing the expression levels of genes associated with extracellular matrix disassembly and contraction. (F) Immunoblotting analysis of ADAM9, α-SMA, SM22α, and p-ERK1/2 expression in MOVAS cells, knockouting Roas26 or Adam9 . (G) Immunoblotting analysis of ADAM9, α-SMA, SM22α, and p-ERK1/2 expression in MOVAS cells with or without treatment of ADAM9 inhibitor (ADAM9i). (H) H to I: Comprehensive profiles of genes in MOVAS cells with treatment of ADAM9i analyzed by bulk RNA-seq. Gene Ontology enrichment analysis of down-regulated genes in MOVAS cells treated with ADAM9i. (I) Heatmap showing the expression levels of metalloprotein genes in MOVAS MOVAS cells in the presence of rhCTHRC1cells treated with ADAM9i or DMSO. (J) Interaction of CTHRC1 with ADAM9 in human aortic smooth muscle cells (HASMCs) confirmed by Co-IP-blotting. (K) Western blotting analysis of ADAM9, α-SMA, SM22α, and p-ERK1/2 expression in HASMCs with treatment of ADAM9i. See also .

Journal: bioRxiv

Article Title: CTHRC1 is a new therapeutic target and serum diagnostic biomarker for aortic dissection

doi: 10.1101/2025.04.19.649636

Figure Lengend Snippet: (A) Workflow of the immunoprecipitation (IP) of CTHRC1 identified by mass spectrometry (MS). (B) Venn diagram of intersection analyses of two independent assays for potential receptors of CTHRC1 on MOVAS cells. Right: Scores of candidate binding proteins identified by MS. (C) Co-IP-blotting of CTHRC1 with ADAM9 receptor on MOVAS cells. (D) D to E: whole transcriptome analysis of MOVAS cells incubated with rhCTHRC1, knockouting Roas26 (control) or Adam9 ( Adam9 -KO). Gene Ontology enrichment analysis of down-regulated genes in Adam9 -KO MOVAS cells treated with rhCTHRC1. (E) Heatmap showing the expression levels of genes associated with extracellular matrix disassembly and contraction. (F) Immunoblotting analysis of ADAM9, α-SMA, SM22α, and p-ERK1/2 expression in MOVAS cells, knockouting Roas26 or Adam9 . (G) Immunoblotting analysis of ADAM9, α-SMA, SM22α, and p-ERK1/2 expression in MOVAS cells with or without treatment of ADAM9 inhibitor (ADAM9i). (H) H to I: Comprehensive profiles of genes in MOVAS cells with treatment of ADAM9i analyzed by bulk RNA-seq. Gene Ontology enrichment analysis of down-regulated genes in MOVAS cells treated with ADAM9i. (I) Heatmap showing the expression levels of metalloprotein genes in MOVAS MOVAS cells in the presence of rhCTHRC1cells treated with ADAM9i or DMSO. (J) Interaction of CTHRC1 with ADAM9 in human aortic smooth muscle cells (HASMCs) confirmed by Co-IP-blotting. (K) Western blotting analysis of ADAM9, α-SMA, SM22α, and p-ERK1/2 expression in HASMCs with treatment of ADAM9i. See also .

Article Snippet: And confluent MOVAS and HASMCs (80%–90%) were treated with recombinant human CTHRC1 Protein (1ug/mL) (HY-P70092, MedChemExpress) to investigate its effect on vascular remodeling in vitro.

Techniques: Immunoprecipitation, Mass Spectrometry, Binding Assay, Co-Immunoprecipitation Assay, Incubation, Control, Expressing, Western Blot, RNA Sequencing

(A) Coomassie staining revealing the protein content in the samples coimmunoprecipitated with CTHRC1. Red box indicates the potential interactors. (B) The representative peptide mass spectrum of ADAM9 receptor on VSMCs. (C) Immunoblotting analysis of ADAM9 in MOVAS incubated with rhCTHRC1 for 0, 3, 6, 12, and 24 hours. (D) Violin plot of Adam9 gene expression in MOVAS cells with treatment of vehicle or rhCTHRC1. (E) Heatmap depicting the gene expression of ADAMs in control and AD mice. (F) F and G: transcriptome analysis of gene expression profiles in MOVAS cells without or with rhCTHRC1, knockouting Roas26 or Adam9 . A volcano plot of differentially expressed genes. The expression levels of Agt , Mmp2 and Mmp9 are down-regulated. (G) KEGG enrichment analysis of down-regulated genes in MOVAS cells in the presence of rhCTHRC1, knockouting Roas26 or Adam9 . (H) Relative mRNA levels of α-SMA and SM22α in MOVAS cells, without or with rhCTHRC1, knockouting Roas26 or Adam9 . (a ordinary one-way ANOVA followed by Bonferroni’s multiple comparison test, ** P ≤ 0.01, *** P ≤ 0.001, **** P ≤ 0.0001.) (I) I to K: Comprehensive profiles of genes in MOVAS cells without or with treatment of ADAM9i by bulk RNA-seq. A volcano plot of differentially expressed genes. Egr1 , Mmp2 and Agt are marked with down-regulated expression. (J) KEGG enrichment analysis of down-regulated genes in MOVAS cells in the presence of rhCTHRC1, with or without ADAM9i. (K) Heatmap showing the expression levels of contraction-related genes in MOVAS cells without or with treatment of ADAM9i, incubated with rhCTHRC1.

Journal: bioRxiv

Article Title: CTHRC1 is a new therapeutic target and serum diagnostic biomarker for aortic dissection

doi: 10.1101/2025.04.19.649636

Figure Lengend Snippet: (A) Coomassie staining revealing the protein content in the samples coimmunoprecipitated with CTHRC1. Red box indicates the potential interactors. (B) The representative peptide mass spectrum of ADAM9 receptor on VSMCs. (C) Immunoblotting analysis of ADAM9 in MOVAS incubated with rhCTHRC1 for 0, 3, 6, 12, and 24 hours. (D) Violin plot of Adam9 gene expression in MOVAS cells with treatment of vehicle or rhCTHRC1. (E) Heatmap depicting the gene expression of ADAMs in control and AD mice. (F) F and G: transcriptome analysis of gene expression profiles in MOVAS cells without or with rhCTHRC1, knockouting Roas26 or Adam9 . A volcano plot of differentially expressed genes. The expression levels of Agt , Mmp2 and Mmp9 are down-regulated. (G) KEGG enrichment analysis of down-regulated genes in MOVAS cells in the presence of rhCTHRC1, knockouting Roas26 or Adam9 . (H) Relative mRNA levels of α-SMA and SM22α in MOVAS cells, without or with rhCTHRC1, knockouting Roas26 or Adam9 . (a ordinary one-way ANOVA followed by Bonferroni’s multiple comparison test, ** P ≤ 0.01, *** P ≤ 0.001, **** P ≤ 0.0001.) (I) I to K: Comprehensive profiles of genes in MOVAS cells without or with treatment of ADAM9i by bulk RNA-seq. A volcano plot of differentially expressed genes. Egr1 , Mmp2 and Agt are marked with down-regulated expression. (J) KEGG enrichment analysis of down-regulated genes in MOVAS cells in the presence of rhCTHRC1, with or without ADAM9i. (K) Heatmap showing the expression levels of contraction-related genes in MOVAS cells without or with treatment of ADAM9i, incubated with rhCTHRC1.

Article Snippet: And confluent MOVAS and HASMCs (80%–90%) were treated with recombinant human CTHRC1 Protein (1ug/mL) (HY-P70092, MedChemExpress) to investigate its effect on vascular remodeling in vitro.

Techniques: Staining, Western Blot, Incubation, Gene Expression, Control, Transcriptome Wide Gene Expression, Expressing, Comparison, RNA Sequencing

(A) Amino acid sequence homology of immunogen with human or mouse CTHRC1 protein. (B) The affinity, specificity, and efficacy of anti-CTHRC1 Ab confirmed by ELISA (left) and immunoblotting (right) analysis. (C) C to E: mRNA sequencing results illustrating the transcriptomic profiles of aortas from WT mice treated with IgG Isotype and anti-CTHRC1 Ab (n=3 per group). PCA of transcriptome profiles in aortic tissues between the two groups. (D) Gene Ontology enrichment analysis of down-regulated genes between the two groups (anti-CTHRC1 Ab versus IgG Isotype). (E) Heatmap showing the expression levels of genes related to vascular smooth muscle cell contraction and extracellular matrix disassembly. (F) F to K: WT female mice were intraperitoneally injected with anti-CTHRC1 Ab or IgG Isotype under saline or Ang-II/BAPN administration (n=10 per group). Kaplan-Meier survival rates analysis of the four groups of female mice. (Kaplan-Meier survival rates analysis, ns, no significance.) (G) Upper: Representative ultrasound images of aorta in female mice (scale bar, 1mm). Bottom: Measurements of maximum aortic diameter of mice (n=6 per group). (Mann Whitney test, *** P ≤ 0.001.) (H) Representative pictures of whole aortas in female mice treated with IgG Isotype or anti-CTHRC1 Ab. (I) Quantification of AD incidence in the whole aorta, ascending, thoracic and abdominal aortas in female mice. (Fisher’s exact test, * P ≤ 0.05.) (J) Representative images of histological staining with hematoxylin and eosin in aortic sections from the female mice. (K) Representative images of EVG staining from the female mice injected with anti-CTHRC1 Ab or IgG Isotype.

Journal: bioRxiv

Article Title: CTHRC1 is a new therapeutic target and serum diagnostic biomarker for aortic dissection

doi: 10.1101/2025.04.19.649636

Figure Lengend Snippet: (A) Amino acid sequence homology of immunogen with human or mouse CTHRC1 protein. (B) The affinity, specificity, and efficacy of anti-CTHRC1 Ab confirmed by ELISA (left) and immunoblotting (right) analysis. (C) C to E: mRNA sequencing results illustrating the transcriptomic profiles of aortas from WT mice treated with IgG Isotype and anti-CTHRC1 Ab (n=3 per group). PCA of transcriptome profiles in aortic tissues between the two groups. (D) Gene Ontology enrichment analysis of down-regulated genes between the two groups (anti-CTHRC1 Ab versus IgG Isotype). (E) Heatmap showing the expression levels of genes related to vascular smooth muscle cell contraction and extracellular matrix disassembly. (F) F to K: WT female mice were intraperitoneally injected with anti-CTHRC1 Ab or IgG Isotype under saline or Ang-II/BAPN administration (n=10 per group). Kaplan-Meier survival rates analysis of the four groups of female mice. (Kaplan-Meier survival rates analysis, ns, no significance.) (G) Upper: Representative ultrasound images of aorta in female mice (scale bar, 1mm). Bottom: Measurements of maximum aortic diameter of mice (n=6 per group). (Mann Whitney test, *** P ≤ 0.001.) (H) Representative pictures of whole aortas in female mice treated with IgG Isotype or anti-CTHRC1 Ab. (I) Quantification of AD incidence in the whole aorta, ascending, thoracic and abdominal aortas in female mice. (Fisher’s exact test, * P ≤ 0.05.) (J) Representative images of histological staining with hematoxylin and eosin in aortic sections from the female mice. (K) Representative images of EVG staining from the female mice injected with anti-CTHRC1 Ab or IgG Isotype.

Article Snippet: And confluent MOVAS and HASMCs (80%–90%) were treated with recombinant human CTHRC1 Protein (1ug/mL) (HY-P70092, MedChemExpress) to investigate its effect on vascular remodeling in vitro.

Techniques: Sequencing, Enzyme-linked Immunosorbent Assay, Western Blot, Expressing, Injection, Saline, MANN-WHITNEY, Staining

(A) The sequences of heavy and light chains from anti-CTHRC1 monoclonal antibody (anti-CTHRC1 Ab), confirmed by variable region cloning, expressing and sequencing. (B) Molecular docking analysis showing the interaction between antibody-CTHRC1 antigen and CTHRC1-ADAM9 receptor at the molecular level. (C) Experiment design. WT mice were intraperitoneally injected with anti-CTHRC1 Ab or IgG Isotype at a dose of 5 μg/g body weight under saline or Ang-II/BAPN administration (n=10 per group). (D) Kaplan-Meier survival rates analysis of the mice treated with anti-CTHRC1 Ab or IgG Isotype under Ang-II/BAPN administration. (Kaplan-Meier survival rates analysis, * P ≤ 0.05, ns, no significance.) (E) Representative ultrasound images of aorta in mice treated with anti-CTHRC1 Ab or IgG Isotype under Ang-II/BAPN administration (scale bar, 1mm). (F) Measurements of maximum aortic diameter of mice in E (n=6-9 per group). (Student’s t-test, ** P ≤ 0.01.) (G) Representative pictures of whole aortas in mice treated with anti-CTHRC1 Ab or IgG Isotype under Ang-II/BAPN administration. The yellow arrows indicate the dissected sites of vascular lesions. (H) Quantification of AD incidence in the whole aorta, ascending, thoracic and abdominal aortas from the mice in E. (Mann-Whitney test, ** P ≤ 0.01.) (I) Representative images of histological staining with hematoxylin and eosin in aortic sections from the mice in E. Bottom: Measurements of aortic wall thickness of aortas (scale bar, 50 μm; scale bar, 200 μm). (Student’s t-test, **** P ≤ 0.00001.) (J) Representative images of Elastica van Gieson staining in aortic sections from the mice in E. Bottom: Numbers of elastin breaks per vessel. (scale bar, 50 μm; scale bar, 200 μm). (Student’s t-test, **** P ≤ 0.00001.) (K) K to O: scRNA-seq of the aortic tissues from WT mice treated with anti-CTHRC1 Ab or IgG Isotype under Ang-II/BAPN administration (n=2 per group). UMAP plot of the 42,623 single cells, displaying the identification of 8 major clusters. (L) The proportion of major cell types including SMCs, ECs and FBs in WT mice treated with anti-CTHRC1 Ab or IgG Isotype under Ang-II/BAPN administration (M) Bar diagram showing the percentage of 4 SMC subclusters in aortic SMCs of the two groups of mice. (N) Boxplot illustrating the differential expression of contractile genes in aortic SMCs of the two groups of mice. (*** P ≤ 0.001, ns, no significance.) (O) Gene Ontology enrichment analysis of differentially down-regulated genes in fibromyocytes of the two groups of mice. (P) Immunoblotting analysis and quantification of α-SMA and SM22α expression in aortas from the WT mice treated with IgG Isotype or anti-CTHRC1 Ab under Ang-II/BAPN infusion (n=6-9). (Student’s t-test, **** P ≤ 0.00001.) See also .

Journal: bioRxiv

Article Title: CTHRC1 is a new therapeutic target and serum diagnostic biomarker for aortic dissection

doi: 10.1101/2025.04.19.649636

Figure Lengend Snippet: (A) The sequences of heavy and light chains from anti-CTHRC1 monoclonal antibody (anti-CTHRC1 Ab), confirmed by variable region cloning, expressing and sequencing. (B) Molecular docking analysis showing the interaction between antibody-CTHRC1 antigen and CTHRC1-ADAM9 receptor at the molecular level. (C) Experiment design. WT mice were intraperitoneally injected with anti-CTHRC1 Ab or IgG Isotype at a dose of 5 μg/g body weight under saline or Ang-II/BAPN administration (n=10 per group). (D) Kaplan-Meier survival rates analysis of the mice treated with anti-CTHRC1 Ab or IgG Isotype under Ang-II/BAPN administration. (Kaplan-Meier survival rates analysis, * P ≤ 0.05, ns, no significance.) (E) Representative ultrasound images of aorta in mice treated with anti-CTHRC1 Ab or IgG Isotype under Ang-II/BAPN administration (scale bar, 1mm). (F) Measurements of maximum aortic diameter of mice in E (n=6-9 per group). (Student’s t-test, ** P ≤ 0.01.) (G) Representative pictures of whole aortas in mice treated with anti-CTHRC1 Ab or IgG Isotype under Ang-II/BAPN administration. The yellow arrows indicate the dissected sites of vascular lesions. (H) Quantification of AD incidence in the whole aorta, ascending, thoracic and abdominal aortas from the mice in E. (Mann-Whitney test, ** P ≤ 0.01.) (I) Representative images of histological staining with hematoxylin and eosin in aortic sections from the mice in E. Bottom: Measurements of aortic wall thickness of aortas (scale bar, 50 μm; scale bar, 200 μm). (Student’s t-test, **** P ≤ 0.00001.) (J) Representative images of Elastica van Gieson staining in aortic sections from the mice in E. Bottom: Numbers of elastin breaks per vessel. (scale bar, 50 μm; scale bar, 200 μm). (Student’s t-test, **** P ≤ 0.00001.) (K) K to O: scRNA-seq of the aortic tissues from WT mice treated with anti-CTHRC1 Ab or IgG Isotype under Ang-II/BAPN administration (n=2 per group). UMAP plot of the 42,623 single cells, displaying the identification of 8 major clusters. (L) The proportion of major cell types including SMCs, ECs and FBs in WT mice treated with anti-CTHRC1 Ab or IgG Isotype under Ang-II/BAPN administration (M) Bar diagram showing the percentage of 4 SMC subclusters in aortic SMCs of the two groups of mice. (N) Boxplot illustrating the differential expression of contractile genes in aortic SMCs of the two groups of mice. (*** P ≤ 0.001, ns, no significance.) (O) Gene Ontology enrichment analysis of differentially down-regulated genes in fibromyocytes of the two groups of mice. (P) Immunoblotting analysis and quantification of α-SMA and SM22α expression in aortas from the WT mice treated with IgG Isotype or anti-CTHRC1 Ab under Ang-II/BAPN infusion (n=6-9). (Student’s t-test, **** P ≤ 0.00001.) See also .

Article Snippet: And confluent MOVAS and HASMCs (80%–90%) were treated with recombinant human CTHRC1 Protein (1ug/mL) (HY-P70092, MedChemExpress) to investigate its effect on vascular remodeling in vitro.

Techniques: Cloning, Expressing, Sequencing, Injection, Saline, MANN-WHITNEY, Staining, Western Blot

(A) A to E: scRNA-seq of aortic tissues in healthy controls and human aortic dissection (n=2 per group). Experiment design of scRNA-seq. (B) Dotplot showing the expression level of CTHRC1 in fibroblasts of the aortas from AD patients and controls. Dash line in each group represents its mean expression value. (C) The proportion of 7 major cell clusters in AD patients and controls. (D) Boxplot displaying the differential gene expression of contractile genes in aortic SMCs of the controls and AD patients. (E) Gene Ontology enrichment analysis of differentially up-regulated genes in fibromyocytes from AD patients versus controls. (F) Heatmap showing the expression levels of genes related to vascular smooth muscle cell contraction and extracellular matrix disassembly in aortic tissues from AD patients and controls by bulk RNA-seq. (*** P ≤ 0.001.) (G) Immunoblotting analysis of CTHRC1, ADAM9, p-ERK1/2 expression levels in human aortas (n=6). (H) Quantification of CTHRC1, ADAM9, p-ERK1/2 protein expression levels in G. (Student’s t-test, ** P ≤ 0.01, **** P ≤ 0.0001.) (I) Immunofluorescence staining of α-SMA and SM22α expression in human aortas (scale bar, 500 μm). (J) Laboratory tests for human serum CTHRC1, cTnT, and D-dimer contents in control individuals, acute myocardial infraction (AMI) and AD. (Student’s t-test, ** P ≤ 0.01, *** P ≤ 0.001, **** P ≤ 0.0001, ns, no significance.) (K) Graphical abstract illustrating an important role of CTHRC1 acts as a candidate circulating biomarker and therapeutic target for aortic dissection through CTRHC1-ADAM9-ERK axis. See also .

Journal: bioRxiv

Article Title: CTHRC1 is a new therapeutic target and serum diagnostic biomarker for aortic dissection

doi: 10.1101/2025.04.19.649636

Figure Lengend Snippet: (A) A to E: scRNA-seq of aortic tissues in healthy controls and human aortic dissection (n=2 per group). Experiment design of scRNA-seq. (B) Dotplot showing the expression level of CTHRC1 in fibroblasts of the aortas from AD patients and controls. Dash line in each group represents its mean expression value. (C) The proportion of 7 major cell clusters in AD patients and controls. (D) Boxplot displaying the differential gene expression of contractile genes in aortic SMCs of the controls and AD patients. (E) Gene Ontology enrichment analysis of differentially up-regulated genes in fibromyocytes from AD patients versus controls. (F) Heatmap showing the expression levels of genes related to vascular smooth muscle cell contraction and extracellular matrix disassembly in aortic tissues from AD patients and controls by bulk RNA-seq. (*** P ≤ 0.001.) (G) Immunoblotting analysis of CTHRC1, ADAM9, p-ERK1/2 expression levels in human aortas (n=6). (H) Quantification of CTHRC1, ADAM9, p-ERK1/2 protein expression levels in G. (Student’s t-test, ** P ≤ 0.01, **** P ≤ 0.0001.) (I) Immunofluorescence staining of α-SMA and SM22α expression in human aortas (scale bar, 500 μm). (J) Laboratory tests for human serum CTHRC1, cTnT, and D-dimer contents in control individuals, acute myocardial infraction (AMI) and AD. (Student’s t-test, ** P ≤ 0.01, *** P ≤ 0.001, **** P ≤ 0.0001, ns, no significance.) (K) Graphical abstract illustrating an important role of CTHRC1 acts as a candidate circulating biomarker and therapeutic target for aortic dissection through CTRHC1-ADAM9-ERK axis. See also .

Article Snippet: And confluent MOVAS and HASMCs (80%–90%) were treated with recombinant human CTHRC1 Protein (1ug/mL) (HY-P70092, MedChemExpress) to investigate its effect on vascular remodeling in vitro.

Techniques: Dissection, Expressing, Gene Expression, RNA Sequencing, Western Blot, Immunofluorescence, Staining, Control, Biomarker Assay

(A) A to E: scRNA-seq data of aortas from human healthy controls and AD patients (n=2 per group). Violin plots showing data characteristics on nFeature, nCount and percent.mt after quality control of the two groups. (B) Violin plot showing the expression level of the housekeeping gene beta-actin (ACTB) of the four samples. The relative stability of ACTB expression indicates consistency. (C) UMAP plot of 45,501 single cells from 4 samples colored according to 7 different cell clusters. (D) UMAP plot of SMCs colored according to the identified 4 SMC subclusters. (E) Bar graphs depicting the numbers of differentially expressed genes in SMC subclusters in healthy controls and AD patients. (F) Gene Ontology enrichment analysis of down-regulated genes in contractile SMCs of the aortas. (G) KEGG enrichment analysis of differentially expressed genes in aortas between the two group. (H) Representative imaging results of contrast-enhanced computed tomography (CT) scanning of patients with aortic dissection, coronary angiography (CAG) of patients with acute myocardial infarction (AMI). The yellow and blue arrows indicate lesion sites in aortas and coronary arteries. (I) Clinical tests for serum biomarkers (Myoglobin, CK-MB, hsCRP and BNP) between AMI or AD patients. (Student’s t-test, * P ≤ 0.05, ** P ≤ 0.01, *** P≤ 0.001, ns, no significance.) (J) A corresponding ELISA kit developed by our team for detecting serum CTHRC1 levels. (K) CTHRC1 point-of-care testing (POCT) equipment, providing rapid and reliable results from a single drop of in less than 10 minutes. (L) The process of assessing chest pain during ambulance transport or in the ER.

Journal: bioRxiv

Article Title: CTHRC1 is a new therapeutic target and serum diagnostic biomarker for aortic dissection

doi: 10.1101/2025.04.19.649636

Figure Lengend Snippet: (A) A to E: scRNA-seq data of aortas from human healthy controls and AD patients (n=2 per group). Violin plots showing data characteristics on nFeature, nCount and percent.mt after quality control of the two groups. (B) Violin plot showing the expression level of the housekeeping gene beta-actin (ACTB) of the four samples. The relative stability of ACTB expression indicates consistency. (C) UMAP plot of 45,501 single cells from 4 samples colored according to 7 different cell clusters. (D) UMAP plot of SMCs colored according to the identified 4 SMC subclusters. (E) Bar graphs depicting the numbers of differentially expressed genes in SMC subclusters in healthy controls and AD patients. (F) Gene Ontology enrichment analysis of down-regulated genes in contractile SMCs of the aortas. (G) KEGG enrichment analysis of differentially expressed genes in aortas between the two group. (H) Representative imaging results of contrast-enhanced computed tomography (CT) scanning of patients with aortic dissection, coronary angiography (CAG) of patients with acute myocardial infarction (AMI). The yellow and blue arrows indicate lesion sites in aortas and coronary arteries. (I) Clinical tests for serum biomarkers (Myoglobin, CK-MB, hsCRP and BNP) between AMI or AD patients. (Student’s t-test, * P ≤ 0.05, ** P ≤ 0.01, *** P≤ 0.001, ns, no significance.) (J) A corresponding ELISA kit developed by our team for detecting serum CTHRC1 levels. (K) CTHRC1 point-of-care testing (POCT) equipment, providing rapid and reliable results from a single drop of in less than 10 minutes. (L) The process of assessing chest pain during ambulance transport or in the ER.

Article Snippet: And confluent MOVAS and HASMCs (80%–90%) were treated with recombinant human CTHRC1 Protein (1ug/mL) (HY-P70092, MedChemExpress) to investigate its effect on vascular remodeling in vitro.

Techniques: Control, Expressing, Imaging, Computed Tomography, Dissection, Enzyme-linked Immunosorbent Assay