adscs  (Dawley Inc)

Journal: Nature Communications

Article Title: Perivascular adipose single-cell atlas identifies CD55 + adipose-derived stem cells as vascular remodeling regulators in atherosclerosis

doi: 10.1038/s41467-026-72962-z

Figure Lengend Snippet: A UMAP visualization of the scRNA-seq profiles showing ADSC subpopulations. B Heatmap of marker genes for CXCL14 + ADSC and CD55 + ADSC cells. C Density maps of CD55 and CXCL14 expression in ADSC subpopulations. D , E Gene Ontology enrichment analysis between the CXCL14 + ADSC and CD55 + ADSC subgroups (biological processes shown). F Violin plots comparing enrichment scores for “positive chemotaxis” and “positive regulation of vascular development” gene sets between CXCL14 + ADSCs and CD55 + ADSCs ( n = 10 patients). Box plots show median, 25th–75th percentiles (box), and 5th–95th percentiles (whiskers). The width of violin plot represents the kernel probability density of the data at different values. G Immunofluorescence staining of CD55 + ADSC (CD142 + CD55 + ) and CXCL14 + ADSC (CD142 + GPC3 + ) in PVAT. Scale bar = 25 μm. H Flow cytometry gating strategy and quantification of CD55 + ADSC (CD45 − CD142 + CD55 + ) and CXCL14 + ADSC (CD45 − CD142 + GPC3 + ) in CAS ( n = 14) vs. control ( n = 7) groups. I Immunofluorescence staining of capillaries (Isolectin B4 + ) and CD55 + ADSC (CD142 + CD55 + ) in PVAT. Scale bar = 30 μm. J Correlation of capillary-positive area (Isolectin B4 + ) between ADSC positive area (CD142 + ) and CD55 + ADSC positive area (CD142 + CD55 + ). K , L Correlation of capillary-positive area (CD31 + ) between ADSC ( n = 84) positive area and CD55 + ADSC ( n = 83) positive area. M Quantification of CD55 + ADSC positive area in asymptomatic ( n = 40) v.s. symptomatic ( n = 49) CAS, and in those with ( n = 31) v.s. without ( n = 58) stroke history. N Quantification of CD31-positive area in asymptomatic ( n = 40) v.s. symptomatic ( n = 53) CAS, and in those with ( n = 29) v.s. without ( n = 71) stroke history. Two-sided Wilcoxon rank-sum test with Benjamini–Hochberg correction was used for analyses in ( F ). Two-tailed unpaired t -test was used for analyses in ( H ). Two-tailed Spearman rank-order correlation analysis with linear regression in ( J – L ). Line: linear regression; shaded area: 95% confidence interval. Two-tailed Mann–Whitney test was used for analyses in ( M ) and ( N ). Representative immunofluorescence images of PVAT from 10 ( G ) and 100 ( I ) patients/samples. Error bars show mean ± SD. Data are presented as individual samples in ( H ) and ( J – N ). UMAP uniform manifold approximation and projection, CAS carotid artery stenosis, PVAT perivascular adipose tissue, ADSC adipose-derived stem cell. Source data are provided as a Source Data file.

Article Snippet: Experimental conditions included a serum-free negative control, a normal medium control, conditioned medium from CD55 + ADSCs (CD55 + ADSC-CM) and CXCL14 + ADSCs (CXCL14 + ADSC-CM), as well as CD55 + ADSC-CM containing 25 nM of the FGFR1 inhibitor PD173074 (HY-10321, MCE, China).

Techniques: Marker, Expressing, Chemotaxis Assay, Immunofluorescence, Staining, Flow Cytometry, Control, Two Tailed Test, MANN-WHITNEY, Derivative Assay

Journal: Nature Communications

Article Title: Perivascular adipose single-cell atlas identifies CD55 + adipose-derived stem cells as vascular remodeling regulators in atherosclerosis

doi: 10.1038/s41467-026-72962-z

Figure Lengend Snippet: A Schematic of carotid partial ligation and intervention experimental procedures in C57 mice and Balb/c nude mice. This schematic was created in BioRender. Chen, J. (2026) https://BioRender.com/4l6sgra . B , C Evaluation of carotid artery remodeling following carotid ligation and murine ADSC transplantation in C57 mice. B Representative EVG staining. C Quantification of neointima and media remodeling across 8 sections (1400 μm span) for CXCL14 + ADSC ( n = 5), CD55 + ADSC ( n = 6), and control ( n = 4) groups. D , E Evaluation of capillary formation (CD31) and ADSC engraftment (GFP) after carotid ligation and murine ADSC transplantation in C57 mice. D Representative images. Scale bar = 50 μm. E Quantification of CD31 + area in ligated arteries. Groups and n values as in ( C ). F – H Vascular remodeling in nude mice after ligation and human ADSC transplantation. F Representative images of Oil Red O staining. Scale bar = 100 μm. G Representative images of EVG staining. Groups and n values as in ( H ). H Quantification of neointima remodeling based on EVG staining (across 8 sections spanning 1400 μm) for CXCL14 + ADSC ( n = 6), CD55 + ADSC ( n = 5), and control ( n = 5) groups. I – L Immunofluorescence assessment of angiogenesis and human ADSC engraftment in nude mice. I , J Representative images of capillary formation (Isolectin B4), human endothelial cell formation (human CD31), and ADSC engraftment (GFP). Scale bar = 100 μm. K Quantification of Isolectin B4 positive area. L Quantification of human CD31-positive area. Groups and n values as in ( H ). M t-SNE visualization and evolutionary tree of lineages from CD55 + ADSC and CXCL14 + ADSC of PVAT to CD31 + endothelial cells of plaque from the same patient with carotid stenosis. Two-tailed two-way ANOVA followed by Tukey’s multiple comparisons test was used for analyses in ( C ) and ( H ). Two-tailed one-way ANOVA followed by Tukey’s multiple comparisons test was used for analyses in ( E , K , and L ). Data are presented as individual samples in ( C , E , H , and K – L ). Data are presented as the mean ± SD. CAS carotid artery stenosis, PVAT perivascular adipose tissue, ADSC adipose-derived stem cell, ns no significance. Source data are provided as a Source Data file.

Article Snippet: Experimental conditions included a serum-free negative control, a normal medium control, conditioned medium from CD55 + ADSCs (CD55 + ADSC-CM) and CXCL14 + ADSCs (CXCL14 + ADSC-CM), as well as CD55 + ADSC-CM containing 25 nM of the FGFR1 inhibitor PD173074 (HY-10321, MCE, China).

Techniques: Ligation, Transplantation Assay, Staining, Control, Immunofluorescence, Two Tailed Test, Derivative Assay

Journal: Nature Communications

Article Title: Perivascular adipose single-cell atlas identifies CD55 + adipose-derived stem cells as vascular remodeling regulators in atherosclerosis

doi: 10.1038/s41467-026-72962-z

Figure Lengend Snippet: During carotid stenosis, the expanded ADSC population includes distinct functional subsets. The CD55 + ADSC subset promotes plaque instability by migrating into lesions, potentially differentiating into endothelial cells, and secreting FGF2 to concurrently stimulate angiogenesis and a synthetic phenotypic switch in smooth muscle cells, resulting in neointimal hyperplasia. Conversely, the CXCL14 + ADSC subset functions in inflammatory recruitment by leveraging pathways like CXCL12-CXCR4 to attract macrophages and other immune cells. Furthermore, extensive cell-cell interactions within PVAT, particularly between these ADSCs and lymphocytes/myeloid cells, orchestrate a synergistic effect that amplifies chemotaxis and angiogenesis, ultimately accelerating the formation of unstable, clinically significant plaques that predispose to stroke. This schematic was created in BioRender. Chen, J. (2026) https://BioRender.com/uf4cxuu .

Article Snippet: Experimental conditions included a serum-free negative control, a normal medium control, conditioned medium from CD55 + ADSCs (CD55 + ADSC-CM) and CXCL14 + ADSCs (CXCL14 + ADSC-CM), as well as CD55 + ADSC-CM containing 25 nM of the FGFR1 inhibitor PD173074 (HY-10321, MCE, China).

Techniques: Functional Assay, Chemotaxis Assay

Journal: Nature Communications

Article Title: Perivascular adipose single-cell atlas identifies CD55 + adipose-derived stem cells as vascular remodeling regulators in atherosclerosis

doi: 10.1038/s41467-026-72962-z

Figure Lengend Snippet: A UMAP visualization of the scRNA-seq profiles showing ADSC subpopulations. B Heatmap of marker genes for CXCL14 + ADSC and CD55 + ADSC cells. C Density maps of CD55 and CXCL14 expression in ADSC subpopulations. D , E Gene Ontology enrichment analysis between the CXCL14 + ADSC and CD55 + ADSC subgroups (biological processes shown). F Violin plots comparing enrichment scores for “positive chemotaxis” and “positive regulation of vascular development” gene sets between CXCL14 + ADSCs and CD55 + ADSCs ( n = 10 patients). Box plots show median, 25th–75th percentiles (box), and 5th–95th percentiles (whiskers). The width of violin plot represents the kernel probability density of the data at different values. G Immunofluorescence staining of CD55 + ADSC (CD142 + CD55 + ) and CXCL14 + ADSC (CD142 + GPC3 + ) in PVAT. Scale bar = 25 μm. H Flow cytometry gating strategy and quantification of CD55 + ADSC (CD45 − CD142 + CD55 + ) and CXCL14 + ADSC (CD45 − CD142 + GPC3 + ) in CAS ( n = 14) vs. control ( n = 7) groups. I Immunofluorescence staining of capillaries (Isolectin B4 + ) and CD55 + ADSC (CD142 + CD55 + ) in PVAT. Scale bar = 30 μm. J Correlation of capillary-positive area (Isolectin B4 + ) between ADSC positive area (CD142 + ) and CD55 + ADSC positive area (CD142 + CD55 + ). K , L Correlation of capillary-positive area (CD31 + ) between ADSC ( n = 84) positive area and CD55 + ADSC ( n = 83) positive area. M Quantification of CD55 + ADSC positive area in asymptomatic ( n = 40) v.s. symptomatic ( n = 49) CAS, and in those with ( n = 31) v.s. without ( n = 58) stroke history. N Quantification of CD31-positive area in asymptomatic ( n = 40) v.s. symptomatic ( n = 53) CAS, and in those with ( n = 29) v.s. without ( n = 71) stroke history. Two-sided Wilcoxon rank-sum test with Benjamini–Hochberg correction was used for analyses in ( F ). Two-tailed unpaired t -test was used for analyses in ( H ). Two-tailed Spearman rank-order correlation analysis with linear regression in ( J – L ). Line: linear regression; shaded area: 95% confidence interval. Two-tailed Mann–Whitney test was used for analyses in ( M ) and ( N ). Representative immunofluorescence images of PVAT from 10 ( G ) and 100 ( I ) patients/samples. Error bars show mean ± SD. Data are presented as individual samples in ( H ) and ( J – N ). UMAP uniform manifold approximation and projection, CAS carotid artery stenosis, PVAT perivascular adipose tissue, ADSC adipose-derived stem cell. Source data are provided as a Source Data file.

Article Snippet: Experimental conditions included a serum-free negative control, a normal medium control, conditioned medium from CD55 + ADSCs (CD55 + ADSC-CM) and CXCL14 + ADSCs (CXCL14 + ADSC-CM), as well as CXCL14 + ADSC-CM containing 10 μM of the CXCR4 inhibitor Plerixafor octahydrochloride (HY-50912, MCE, China).

Techniques: Marker, Expressing, Chemotaxis Assay, Immunofluorescence, Staining, Flow Cytometry, Control, Two Tailed Test, MANN-WHITNEY, Derivative Assay

Journal: Nature Communications

Article Title: Perivascular adipose single-cell atlas identifies CD55 + adipose-derived stem cells as vascular remodeling regulators in atherosclerosis

doi: 10.1038/s41467-026-72962-z

Figure Lengend Snippet: A Schematic of carotid partial ligation and intervention experimental procedures in C57 mice and Balb/c nude mice. This schematic was created in BioRender. Chen, J. (2026) https://BioRender.com/4l6sgra . B , C Evaluation of carotid artery remodeling following carotid ligation and murine ADSC transplantation in C57 mice. B Representative EVG staining. C Quantification of neointima and media remodeling across 8 sections (1400 μm span) for CXCL14 + ADSC ( n = 5), CD55 + ADSC ( n = 6), and control ( n = 4) groups. D , E Evaluation of capillary formation (CD31) and ADSC engraftment (GFP) after carotid ligation and murine ADSC transplantation in C57 mice. D Representative images. Scale bar = 50 μm. E Quantification of CD31 + area in ligated arteries. Groups and n values as in ( C ). F – H Vascular remodeling in nude mice after ligation and human ADSC transplantation. F Representative images of Oil Red O staining. Scale bar = 100 μm. G Representative images of EVG staining. Groups and n values as in ( H ). H Quantification of neointima remodeling based on EVG staining (across 8 sections spanning 1400 μm) for CXCL14 + ADSC ( n = 6), CD55 + ADSC ( n = 5), and control ( n = 5) groups. I – L Immunofluorescence assessment of angiogenesis and human ADSC engraftment in nude mice. I , J Representative images of capillary formation (Isolectin B4), human endothelial cell formation (human CD31), and ADSC engraftment (GFP). Scale bar = 100 μm. K Quantification of Isolectin B4 positive area. L Quantification of human CD31-positive area. Groups and n values as in ( H ). M t-SNE visualization and evolutionary tree of lineages from CD55 + ADSC and CXCL14 + ADSC of PVAT to CD31 + endothelial cells of plaque from the same patient with carotid stenosis. Two-tailed two-way ANOVA followed by Tukey’s multiple comparisons test was used for analyses in ( C ) and ( H ). Two-tailed one-way ANOVA followed by Tukey’s multiple comparisons test was used for analyses in ( E , K , and L ). Data are presented as individual samples in ( C , E , H , and K – L ). Data are presented as the mean ± SD. CAS carotid artery stenosis, PVAT perivascular adipose tissue, ADSC adipose-derived stem cell, ns no significance. Source data are provided as a Source Data file.

Article Snippet: Experimental conditions included a serum-free negative control, a normal medium control, conditioned medium from CD55 + ADSCs (CD55 + ADSC-CM) and CXCL14 + ADSCs (CXCL14 + ADSC-CM), as well as CXCL14 + ADSC-CM containing 10 μM of the CXCR4 inhibitor Plerixafor octahydrochloride (HY-50912, MCE, China).

Techniques: Ligation, Transplantation Assay, Staining, Control, Immunofluorescence, Two Tailed Test, Derivative Assay

Journal: Nature Communications

Article Title: Perivascular adipose single-cell atlas identifies CD55 + adipose-derived stem cells as vascular remodeling regulators in atherosclerosis

doi: 10.1038/s41467-026-72962-z

Figure Lengend Snippet: A Cell-cell crosstalk analysis among ADSC subsets and T cell subpopulation interaction weights in control v.s. CAS groups. B Outgoing-Incoming interaction strength analysis among ADSC subsets and T cell subpopulations in control v.s. CAS groups. C Interaction strength difference analysis among ADSC subsets and T cell subpopulations in control v.s. CAS groups. D Cell-cell crosstalk analysis among ADSC subsets and myeloid cell subpopulation interaction weights in control v.s. CAS groups. E Outgoing-Incoming interaction strength analysis among ADSC subsets and myeloid cell subpopulations in control v.s. CAS groups. F Interaction strength difference analysis among ADSC subsets and myeloid cell subpopulations in control v.s. CAS groups. G Ligand-receptor bubble plot of increased communication from ADSC subtypes to T cell subpopulations. H Ligand-receptor bubble plot of increased communication from ADSC subtypes to myeloid subtypes. I Chordal chart of CXCL12-CXCR4 pathway communication strength among ADSC subtypes, myeloid cell subtypes, NK cell subtypes, and T cell subtypes in CAS group and/or control group. J ELISA test detecting the expression level of CXCL12 in ADSC-conditioned medium. Experiments were performed with three biological replicates. K ELISA test detecting the expression level of CXCL14 in ADSC-conditioned medium. Experiments were performed with three biological replicates. L – N Representative images and statistical analysis of Transwell assay, examining whether CXCL14⁺ADSCs recruit macrophages via the CXCL12-CXCR4 pathway. Scale bar = 50 μm. Experiments were performed with six biological replicates. O Chordal chart of AREG-EGFR pathway communication strength among ADSC subtypes, myeloid cell subtypes, NK cell subtypes, and T cell subtypes in CAS group and/or control group. P –values in ( G ) and ( H ) were calculated using one-sided permutation tests without correction for multiple comparisons. Two-tailed unpaired t -test was used for ( J , K , and N ). Error bars show mean ± SD. CAS carotid artery stenosis, ADSC adipose-derived stem cell. Source data are provided as a Source Data file.

Article Snippet: Experimental conditions included a serum-free negative control, a normal medium control, conditioned medium from CD55 + ADSCs (CD55 + ADSC-CM) and CXCL14 + ADSCs (CXCL14 + ADSC-CM), as well as CXCL14 + ADSC-CM containing 10 μM of the CXCR4 inhibitor Plerixafor octahydrochloride (HY-50912, MCE, China).

Techniques: Control, Enzyme-linked Immunosorbent Assay, Expressing, Transwell Assay, Two Tailed Test, Derivative Assay

Journal: Nature Communications

Article Title: Perivascular adipose single-cell atlas identifies CD55 + adipose-derived stem cells as vascular remodeling regulators in atherosclerosis

doi: 10.1038/s41467-026-72962-z

Figure Lengend Snippet: During carotid stenosis, the expanded ADSC population includes distinct functional subsets. The CD55 + ADSC subset promotes plaque instability by migrating into lesions, potentially differentiating into endothelial cells, and secreting FGF2 to concurrently stimulate angiogenesis and a synthetic phenotypic switch in smooth muscle cells, resulting in neointimal hyperplasia. Conversely, the CXCL14 + ADSC subset functions in inflammatory recruitment by leveraging pathways like CXCL12-CXCR4 to attract macrophages and other immune cells. Furthermore, extensive cell-cell interactions within PVAT, particularly between these ADSCs and lymphocytes/myeloid cells, orchestrate a synergistic effect that amplifies chemotaxis and angiogenesis, ultimately accelerating the formation of unstable, clinically significant plaques that predispose to stroke. This schematic was created in BioRender. Chen, J. (2026) https://BioRender.com/uf4cxuu .

Article Snippet: Experimental conditions included a serum-free negative control, a normal medium control, conditioned medium from CD55 + ADSCs (CD55 + ADSC-CM) and CXCL14 + ADSCs (CXCL14 + ADSC-CM), as well as CXCL14 + ADSC-CM containing 10 μM of the CXCR4 inhibitor Plerixafor octahydrochloride (HY-50912, MCE, China).

Techniques: Functional Assay, Chemotaxis Assay