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Spatial Transcriptomics Inc 10x visium spatial transcriptomics slide
(a) MI was induced followed by an intramyocardial injection of ECM hydrogel or saline 7 days post-MI. Hearts were then harvested for either snRNAseq or spatial <t>transcriptomics</t> 7 days post-injection (14 days post-MI). Sample size: n = 2 ECM hydrogel replicates, 7658 spots. (b) Myocardium (green) was labelled with anti-alpha-actinin antibody alongside fluorescently tagged ECM hydrogel (light blue). (c) The adjacent cryosection was used for spatial transcriptomics via <t>10X</t> <t>Visium,</t> where the infarct containing ECM hydrogel (red) was found to cluster separately from the infarct alone (cyan). (d) The top upregulated differentially expressed genes defining the ECM hydrogel zone (red) were found to be immune and vascularly dominating genes compared to the down regulated genes impacting the infarct zone (cyan). (e-f) All differentially expressed genes in the ECM hydrogel zone (red) and infarct only zone were subjected to GO enrichment.
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1) Product Images from "Uncovering the Regional and Cell Specific Bioactivity of Injectable Extracellular Matrix Biomaterials in Myocardial Infarction through Spatial and Single Nucleus Transcriptomics"

Article Title: Uncovering the Regional and Cell Specific Bioactivity of Injectable Extracellular Matrix Biomaterials in Myocardial Infarction through Spatial and Single Nucleus Transcriptomics

Journal: bioRxiv

doi: 10.1101/2025.06.25.661525

(a) MI was induced followed by an intramyocardial injection of ECM hydrogel or saline 7 days post-MI. Hearts were then harvested for either snRNAseq or spatial transcriptomics 7 days post-injection (14 days post-MI). Sample size: n = 2 ECM hydrogel replicates, 7658 spots. (b) Myocardium (green) was labelled with anti-alpha-actinin antibody alongside fluorescently tagged ECM hydrogel (light blue). (c) The adjacent cryosection was used for spatial transcriptomics via 10X Visium, where the infarct containing ECM hydrogel (red) was found to cluster separately from the infarct alone (cyan). (d) The top upregulated differentially expressed genes defining the ECM hydrogel zone (red) were found to be immune and vascularly dominating genes compared to the down regulated genes impacting the infarct zone (cyan). (e-f) All differentially expressed genes in the ECM hydrogel zone (red) and infarct only zone were subjected to GO enrichment.
Figure Legend Snippet: (a) MI was induced followed by an intramyocardial injection of ECM hydrogel or saline 7 days post-MI. Hearts were then harvested for either snRNAseq or spatial transcriptomics 7 days post-injection (14 days post-MI). Sample size: n = 2 ECM hydrogel replicates, 7658 spots. (b) Myocardium (green) was labelled with anti-alpha-actinin antibody alongside fluorescently tagged ECM hydrogel (light blue). (c) The adjacent cryosection was used for spatial transcriptomics via 10X Visium, where the infarct containing ECM hydrogel (red) was found to cluster separately from the infarct alone (cyan). (d) The top upregulated differentially expressed genes defining the ECM hydrogel zone (red) were found to be immune and vascularly dominating genes compared to the down regulated genes impacting the infarct zone (cyan). (e-f) All differentially expressed genes in the ECM hydrogel zone (red) and infarct only zone were subjected to GO enrichment.

Techniques Used: Injection, Saline

(a) MI is induced followed by an intramyocardial injection of ECM hydrogel or saline 8 weeks post-MI. Hearts are then harvested for either snRNAseq or spatial transcriptomics 7 days post-injection. Sample size: n = 3 ECM hydrogel replicates, 9594 spots. (b) Myocardium (green) was labelled with an anti-alpha-actinin antibody alongside fluorescently tagged ECM hydrogel (light blue). (c) An adjacent cryosection to the immunofluorescence image in b was used for spatial transcriptomics via 10X Visium, where the infarct containing ECM hydrogel (red) was found to cluster separately from the normal infarct zone (cyan). (d) Top differentially expressed genes for both ECM within infarct (red) and infarct alone (cyan) are shown. (e-f) A comparison of the two zones reflects the ECM hydrogel activates fibroblasts and is responsible for further vascular development, as demonstrated through GO enrichment.
Figure Legend Snippet: (a) MI is induced followed by an intramyocardial injection of ECM hydrogel or saline 8 weeks post-MI. Hearts are then harvested for either snRNAseq or spatial transcriptomics 7 days post-injection. Sample size: n = 3 ECM hydrogel replicates, 9594 spots. (b) Myocardium (green) was labelled with an anti-alpha-actinin antibody alongside fluorescently tagged ECM hydrogel (light blue). (c) An adjacent cryosection to the immunofluorescence image in b was used for spatial transcriptomics via 10X Visium, where the infarct containing ECM hydrogel (red) was found to cluster separately from the normal infarct zone (cyan). (d) Top differentially expressed genes for both ECM within infarct (red) and infarct alone (cyan) are shown. (e-f) A comparison of the two zones reflects the ECM hydrogel activates fibroblasts and is responsible for further vascular development, as demonstrated through GO enrichment.

Techniques Used: Injection, Saline, Immunofluorescence, Comparison

(a) The top upregulated differentially expressed genes defining the ECM hydrogel zone (red) with integrated subacute and chronic Visium were found to be immune, fibroblast, and vascularly dominating genes compared to the downregulated genes impacting the infarct zone (cyan). Sample size: n = 2 for subacute ECM hydrogel (7658 spots); n = 3 for chronic ECM hydrogel (9594 spots) (b) The ECM zones in both subacute and chronic models of MI have higher expression of the matrix specific genes relative to the infarct zone. (c-f) Macrophages (c) , endothelial cells (d) , cardiomyocytes (e) , and fibroblasts (f) treated with ECM hydrogel in subacute and chronic MI were subsetted, reclustered and compared with respect to MI timepoint. Sample size: n = 2 subacute ECM hydrogel (downsampled to 3000 cells), n = 2 chronic ECM hydrogel (downsampled to 3000 cells). Top differentially expressed genes were displayed via Volcano Plot, and the differentially expressed genes were subjected to GO enrichment. (g) Comparison of transcriptomic findings between subacute and chronic MI.
Figure Legend Snippet: (a) The top upregulated differentially expressed genes defining the ECM hydrogel zone (red) with integrated subacute and chronic Visium were found to be immune, fibroblast, and vascularly dominating genes compared to the downregulated genes impacting the infarct zone (cyan). Sample size: n = 2 for subacute ECM hydrogel (7658 spots); n = 3 for chronic ECM hydrogel (9594 spots) (b) The ECM zones in both subacute and chronic models of MI have higher expression of the matrix specific genes relative to the infarct zone. (c-f) Macrophages (c) , endothelial cells (d) , cardiomyocytes (e) , and fibroblasts (f) treated with ECM hydrogel in subacute and chronic MI were subsetted, reclustered and compared with respect to MI timepoint. Sample size: n = 2 subacute ECM hydrogel (downsampled to 3000 cells), n = 2 chronic ECM hydrogel (downsampled to 3000 cells). Top differentially expressed genes were displayed via Volcano Plot, and the differentially expressed genes were subjected to GO enrichment. (g) Comparison of transcriptomic findings between subacute and chronic MI.

Techniques Used: Expressing, Comparison



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Spatial Transcriptomics Inc 10x visium spatial transcriptomics slide
(a) MI was induced followed by an intramyocardial injection of ECM hydrogel or saline 7 days post-MI. Hearts were then harvested for either snRNAseq or spatial <t>transcriptomics</t> 7 days post-injection (14 days post-MI). Sample size: n = 2 ECM hydrogel replicates, 7658 spots. (b) Myocardium (green) was labelled with anti-alpha-actinin antibody alongside fluorescently tagged ECM hydrogel (light blue). (c) The adjacent cryosection was used for spatial transcriptomics via <t>10X</t> <t>Visium,</t> where the infarct containing ECM hydrogel (red) was found to cluster separately from the infarct alone (cyan). (d) The top upregulated differentially expressed genes defining the ECM hydrogel zone (red) were found to be immune and vascularly dominating genes compared to the down regulated genes impacting the infarct zone (cyan). (e-f) All differentially expressed genes in the ECM hydrogel zone (red) and infarct only zone were subjected to GO enrichment.
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(a) MI was induced followed by an intramyocardial injection of ECM hydrogel or saline 7 days post-MI. Hearts were then harvested for either snRNAseq or spatial <t>transcriptomics</t> 7 days post-injection (14 days post-MI). Sample size: n = 2 ECM hydrogel replicates, 7658 spots. (b) Myocardium (green) was labelled with anti-alpha-actinin antibody alongside fluorescently tagged ECM hydrogel (light blue). (c) The adjacent cryosection was used for spatial transcriptomics via <t>10X</t> <t>Visium,</t> where the infarct containing ECM hydrogel (red) was found to cluster separately from the infarct alone (cyan). (d) The top upregulated differentially expressed genes defining the ECM hydrogel zone (red) were found to be immune and vascularly dominating genes compared to the down regulated genes impacting the infarct zone (cyan). (e-f) All differentially expressed genes in the ECM hydrogel zone (red) and infarct only zone were subjected to GO enrichment.
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(a) MI was induced followed by an intramyocardial injection of ECM hydrogel or saline 7 days post-MI. Hearts were then harvested for either snRNAseq or spatial <t>transcriptomics</t> 7 days post-injection (14 days post-MI). Sample size: n = 2 ECM hydrogel replicates, 7658 spots. (b) Myocardium (green) was labelled with anti-alpha-actinin antibody alongside fluorescently tagged ECM hydrogel (light blue). (c) The adjacent cryosection was used for spatial transcriptomics via <t>10X</t> <t>Visium,</t> where the infarct containing ECM hydrogel (red) was found to cluster separately from the infarct alone (cyan). (d) The top upregulated differentially expressed genes defining the ECM hydrogel zone (red) were found to be immune and vascularly dominating genes compared to the down regulated genes impacting the infarct zone (cyan). (e-f) All differentially expressed genes in the ECM hydrogel zone (red) and infarct only zone were subjected to GO enrichment.
Visium Spatial Transcriptomic Slide, supplied by 10X Genomics, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/result/visium spatial transcriptomic slide/product/10X Genomics
Average 90 stars, based on 1 article reviews
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Wound healing in Atlantic salmon. a Histological micrographs depicting incisional wound at 2 days post-wounding (DPW), with Alcian blue and periodic acid-Schiff (PAS) staining to facilitate viewing of the incisional wound during the inflammation stage b Histological micrographs depicting incisional wound at 14 DPW, with Movat staining to facilitate viewing of the granulation tissue during the remodelling stage. c - f <t>10x</t> <t>Visium</t> Spatial <t>Transcriptomics</t> Slides. Expression of putative pure MSC population 2 top 20 transcript from Seurat snRNA-seq data (Additional file 1: Table S10) at 2 DPW and 14 DPW ( c , d ). Expression of putative pure MSC population 1 top 20 transcripts from PHATE snRNA-seq analysis (Additional file 1: Table S10) at 2 DPW and 14 DPW ( e , f ). Wound bed (Wb), epidermis (Epi), dense connective tissue (Dct), skeletal muscle fibres (Mu), damaged white muscle fibres (Mu*), myosepta (Myo) and newly formed epithelial tissue (“Neo Epi”). Scales (Sc), adipose tissue (Adi), polymorphonucleated inflammatory cells (InF), granulation tissue (Gt), blood vessel formation (Bv) and fibril formation (Ff). Scale bars: 500 µm ( a – f ). The colour of the scale in c - f indicates the expression of transcripts mapped on the slide from low (blue) to high (red)
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Spatial Transcriptomics Inc spatial transcriptomics slides visium 10x
Cold fibrosis after MI is conserved in humans and in a clinically relevant porcine model (A and B) (A) Representative human left ventricle spatial <t>transcriptomics</t> slides (Visium) of patients following acute-myocardial infarction (MI) and non-transplanted donor hearts. Samples were divided based on time following MI as either: uninjured ( n = 10), early (days 0–15 post-MI; n = 6), and late (30 days+; n = 6). (B) Abundance of fibroblasts and myeloid cells was quantified based on deconvolution scores of cell types per spot . Myofibroblast were calculated as enrichment of the mean myofibroblast state score within spots with a minimal 10% value of cell-type abundance . Statistical analysis used Wilcoxon tests with Benjamini-Hochberg adjusted p values. (C) Experimental design of pig MI experiment: adult (3 months old) pigs underwent MI by temporarily occluding their LAD using a balloon catheter . Following reperfusion (balloon deflation), pigs were immediately treated with recombinant human Agrin (rhAgrin) or Saline control, in an antegrade trajectory. Injured pig hearts were collected at either day 3 ( n = 4 for rhAgrin; n = 3 for Saline) or day 28 ( n = 4 for rhAgrin; n = 3 for saline) and dissected to distinct tissue areas (infarct and remote zones). Remote and infarcted samples were subjected to bulk-mRNA sequencing and histology for fibrosis assessment. (D and E) Representative sirius red staining images are shown from (D) day 3 and (E) day 28 post-MI. Fibrosis was quantified as the average % fold change (FC) between infarct/remote zone sections for each pig individually. Fibrosis (day 3 or day 28) for Saline and rhAgrin hearts was measured using two-tailed unpaired t test. Scale bars: 1 mm. striated line denotes FC = 1. n.s, non-significant difference. (F and G) Heatmaps based on log 2 transformed normalized counts for all (upregulated and downregulated) differentially expressed genes (defined by |log 2 fold change| ≥ 1, p -adjusted value < 0.05 and max raw counts > 30) between remote and infarct zones for Saline and rhAgrin-treated hearts at day 3 (5,961 genes) (F) and 28 (1,079 genes) (G) post-MI. Rows represent genes and columns represent each biological sample and its spatial distribution according to infarct or remote zone. Data are represented as mean ± SD. (H) Hierarchical clustering per condition (day [3 or 28] +treatment [rhAgrin or Saline]), based on the 1,000 most variable genes. Triangles and circles represent remote and infarct zones, respectively. (I) Deconvolution of bulk-mRNA sequencing of pig hearts following MI of either rhAgrin (blue) or Saline-treated (red) samples. Macrophage and myofibroblast abundances were assessed by gene signatures as FC, between infarct and remote zones ( , C, and <xref ref-type=Table S5 ). (J) Macrophage and myofibroblast abundances, based on deconvolution of bulk-mRNA sequencing (as in I). Treated samples were compared per time point (day 3 or 28), separately by two-tailed unpaired Student t test. Results are represented as mean ± SEM. " width="250" height="auto" />
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( A ) Violin plots showing expression of canonical marker genes in different endometrial cell types. ( B ) Violin plots showing PLA2G2A and DIO2 expression across different endometrial cell types with p -values based on Wilcoxon rank sum test; a.u., arbitrary units. ( C ) Column bar graphs depicting the relative abundance of stromal subsets across the indicated cycle days. ( D ) RNA velocity mapped onto UMAP plots of stromal subsets in nine endometrial biopsies. ( E ) Visualization of the GSEA hallmark ‘DNA Repair’ gene set in mid-luteal endometrium by <t>Visium</t> spatial <t>transcriptomics</t> (upper panel). The lower panel shows the corresponding tissue section stained with H&E.
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( A ) Violin plots showing expression of canonical marker genes in different endometrial cell types. ( B ) Violin plots showing PLA2G2A and DIO2 expression across different endometrial cell types with p -values based on Wilcoxon rank sum test; a.u., arbitrary units. ( C ) Column bar graphs depicting the relative abundance of stromal subsets across the indicated cycle days. ( D ) RNA velocity mapped onto UMAP plots of stromal subsets in nine endometrial biopsies. ( E ) Visualization of the GSEA hallmark ‘DNA Repair’ gene set in mid-luteal endometrium by <t>Visium</t> spatial <t>transcriptomics</t> (upper panel). The lower panel shows the corresponding tissue section stained with H&E.
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(a) MI was induced followed by an intramyocardial injection of ECM hydrogel or saline 7 days post-MI. Hearts were then harvested for either snRNAseq or spatial transcriptomics 7 days post-injection (14 days post-MI). Sample size: n = 2 ECM hydrogel replicates, 7658 spots. (b) Myocardium (green) was labelled with anti-alpha-actinin antibody alongside fluorescently tagged ECM hydrogel (light blue). (c) The adjacent cryosection was used for spatial transcriptomics via 10X Visium, where the infarct containing ECM hydrogel (red) was found to cluster separately from the infarct alone (cyan). (d) The top upregulated differentially expressed genes defining the ECM hydrogel zone (red) were found to be immune and vascularly dominating genes compared to the down regulated genes impacting the infarct zone (cyan). (e-f) All differentially expressed genes in the ECM hydrogel zone (red) and infarct only zone were subjected to GO enrichment.

Journal: bioRxiv

Article Title: Uncovering the Regional and Cell Specific Bioactivity of Injectable Extracellular Matrix Biomaterials in Myocardial Infarction through Spatial and Single Nucleus Transcriptomics

doi: 10.1101/2025.06.25.661525

Figure Lengend Snippet: (a) MI was induced followed by an intramyocardial injection of ECM hydrogel or saline 7 days post-MI. Hearts were then harvested for either snRNAseq or spatial transcriptomics 7 days post-injection (14 days post-MI). Sample size: n = 2 ECM hydrogel replicates, 7658 spots. (b) Myocardium (green) was labelled with anti-alpha-actinin antibody alongside fluorescently tagged ECM hydrogel (light blue). (c) The adjacent cryosection was used for spatial transcriptomics via 10X Visium, where the infarct containing ECM hydrogel (red) was found to cluster separately from the infarct alone (cyan). (d) The top upregulated differentially expressed genes defining the ECM hydrogel zone (red) were found to be immune and vascularly dominating genes compared to the down regulated genes impacting the infarct zone (cyan). (e-f) All differentially expressed genes in the ECM hydrogel zone (red) and infarct only zone were subjected to GO enrichment.

Article Snippet: Odd slices were frozen in TissueTek OCT TM and sectioned into 10 μm thick slices and placed onto a 10X Visium Spatial Transcriptomics Slide or a regular histology slide.

Techniques: Injection, Saline

(a) MI is induced followed by an intramyocardial injection of ECM hydrogel or saline 8 weeks post-MI. Hearts are then harvested for either snRNAseq or spatial transcriptomics 7 days post-injection. Sample size: n = 3 ECM hydrogel replicates, 9594 spots. (b) Myocardium (green) was labelled with an anti-alpha-actinin antibody alongside fluorescently tagged ECM hydrogel (light blue). (c) An adjacent cryosection to the immunofluorescence image in b was used for spatial transcriptomics via 10X Visium, where the infarct containing ECM hydrogel (red) was found to cluster separately from the normal infarct zone (cyan). (d) Top differentially expressed genes for both ECM within infarct (red) and infarct alone (cyan) are shown. (e-f) A comparison of the two zones reflects the ECM hydrogel activates fibroblasts and is responsible for further vascular development, as demonstrated through GO enrichment.

Journal: bioRxiv

Article Title: Uncovering the Regional and Cell Specific Bioactivity of Injectable Extracellular Matrix Biomaterials in Myocardial Infarction through Spatial and Single Nucleus Transcriptomics

doi: 10.1101/2025.06.25.661525

Figure Lengend Snippet: (a) MI is induced followed by an intramyocardial injection of ECM hydrogel or saline 8 weeks post-MI. Hearts are then harvested for either snRNAseq or spatial transcriptomics 7 days post-injection. Sample size: n = 3 ECM hydrogel replicates, 9594 spots. (b) Myocardium (green) was labelled with an anti-alpha-actinin antibody alongside fluorescently tagged ECM hydrogel (light blue). (c) An adjacent cryosection to the immunofluorescence image in b was used for spatial transcriptomics via 10X Visium, where the infarct containing ECM hydrogel (red) was found to cluster separately from the normal infarct zone (cyan). (d) Top differentially expressed genes for both ECM within infarct (red) and infarct alone (cyan) are shown. (e-f) A comparison of the two zones reflects the ECM hydrogel activates fibroblasts and is responsible for further vascular development, as demonstrated through GO enrichment.

Article Snippet: Odd slices were frozen in TissueTek OCT TM and sectioned into 10 μm thick slices and placed onto a 10X Visium Spatial Transcriptomics Slide or a regular histology slide.

Techniques: Injection, Saline, Immunofluorescence, Comparison

(a) The top upregulated differentially expressed genes defining the ECM hydrogel zone (red) with integrated subacute and chronic Visium were found to be immune, fibroblast, and vascularly dominating genes compared to the downregulated genes impacting the infarct zone (cyan). Sample size: n = 2 for subacute ECM hydrogel (7658 spots); n = 3 for chronic ECM hydrogel (9594 spots) (b) The ECM zones in both subacute and chronic models of MI have higher expression of the matrix specific genes relative to the infarct zone. (c-f) Macrophages (c) , endothelial cells (d) , cardiomyocytes (e) , and fibroblasts (f) treated with ECM hydrogel in subacute and chronic MI were subsetted, reclustered and compared with respect to MI timepoint. Sample size: n = 2 subacute ECM hydrogel (downsampled to 3000 cells), n = 2 chronic ECM hydrogel (downsampled to 3000 cells). Top differentially expressed genes were displayed via Volcano Plot, and the differentially expressed genes were subjected to GO enrichment. (g) Comparison of transcriptomic findings between subacute and chronic MI.

Journal: bioRxiv

Article Title: Uncovering the Regional and Cell Specific Bioactivity of Injectable Extracellular Matrix Biomaterials in Myocardial Infarction through Spatial and Single Nucleus Transcriptomics

doi: 10.1101/2025.06.25.661525

Figure Lengend Snippet: (a) The top upregulated differentially expressed genes defining the ECM hydrogel zone (red) with integrated subacute and chronic Visium were found to be immune, fibroblast, and vascularly dominating genes compared to the downregulated genes impacting the infarct zone (cyan). Sample size: n = 2 for subacute ECM hydrogel (7658 spots); n = 3 for chronic ECM hydrogel (9594 spots) (b) The ECM zones in both subacute and chronic models of MI have higher expression of the matrix specific genes relative to the infarct zone. (c-f) Macrophages (c) , endothelial cells (d) , cardiomyocytes (e) , and fibroblasts (f) treated with ECM hydrogel in subacute and chronic MI were subsetted, reclustered and compared with respect to MI timepoint. Sample size: n = 2 subacute ECM hydrogel (downsampled to 3000 cells), n = 2 chronic ECM hydrogel (downsampled to 3000 cells). Top differentially expressed genes were displayed via Volcano Plot, and the differentially expressed genes were subjected to GO enrichment. (g) Comparison of transcriptomic findings between subacute and chronic MI.

Article Snippet: Odd slices were frozen in TissueTek OCT TM and sectioned into 10 μm thick slices and placed onto a 10X Visium Spatial Transcriptomics Slide or a regular histology slide.

Techniques: Expressing, Comparison

Wound healing in Atlantic salmon. a Histological micrographs depicting incisional wound at 2 days post-wounding (DPW), with Alcian blue and periodic acid-Schiff (PAS) staining to facilitate viewing of the incisional wound during the inflammation stage b Histological micrographs depicting incisional wound at 14 DPW, with Movat staining to facilitate viewing of the granulation tissue during the remodelling stage. c - f 10x Visium Spatial Transcriptomics Slides. Expression of putative pure MSC population 2 top 20 transcript from Seurat snRNA-seq data (Additional file 1: Table S10) at 2 DPW and 14 DPW ( c , d ). Expression of putative pure MSC population 1 top 20 transcripts from PHATE snRNA-seq analysis (Additional file 1: Table S10) at 2 DPW and 14 DPW ( e , f ). Wound bed (Wb), epidermis (Epi), dense connective tissue (Dct), skeletal muscle fibres (Mu), damaged white muscle fibres (Mu*), myosepta (Myo) and newly formed epithelial tissue (“Neo Epi”). Scales (Sc), adipose tissue (Adi), polymorphonucleated inflammatory cells (InF), granulation tissue (Gt), blood vessel formation (Bv) and fibril formation (Ff). Scale bars: 500 µm ( a – f ). The colour of the scale in c - f indicates the expression of transcripts mapped on the slide from low (blue) to high (red)

Journal: BMC Biology

Article Title: Transcriptomic characterization of transitioning cell types in the skin of Atlantic salmon

doi: 10.1186/s12915-025-02196-w

Figure Lengend Snippet: Wound healing in Atlantic salmon. a Histological micrographs depicting incisional wound at 2 days post-wounding (DPW), with Alcian blue and periodic acid-Schiff (PAS) staining to facilitate viewing of the incisional wound during the inflammation stage b Histological micrographs depicting incisional wound at 14 DPW, with Movat staining to facilitate viewing of the granulation tissue during the remodelling stage. c - f 10x Visium Spatial Transcriptomics Slides. Expression of putative pure MSC population 2 top 20 transcript from Seurat snRNA-seq data (Additional file 1: Table S10) at 2 DPW and 14 DPW ( c , d ). Expression of putative pure MSC population 1 top 20 transcripts from PHATE snRNA-seq analysis (Additional file 1: Table S10) at 2 DPW and 14 DPW ( e , f ). Wound bed (Wb), epidermis (Epi), dense connective tissue (Dct), skeletal muscle fibres (Mu), damaged white muscle fibres (Mu*), myosepta (Myo) and newly formed epithelial tissue (“Neo Epi”). Scales (Sc), adipose tissue (Adi), polymorphonucleated inflammatory cells (InF), granulation tissue (Gt), blood vessel formation (Bv) and fibril formation (Ff). Scale bars: 500 µm ( a – f ). The colour of the scale in c - f indicates the expression of transcripts mapped on the slide from low (blue) to high (red)

Article Snippet: Fig. 5 Wound healing in Atlantic salmon. a Histological micrographs depicting incisional wound at 2 days post-wounding (DPW), with Alcian blue and periodic acid-Schiff (PAS) staining to facilitate viewing of the incisional wound during the inflammation stage b Histological micrographs depicting incisional wound at 14 DPW, with Movat staining to facilitate viewing of the granulation tissue during the remodelling stage. c - f 10x Visium Spatial Transcriptomics Slides.

Techniques: Staining, Expressing

Charting the transcriptomic activity of different putative MSC-associated subclusters (10x Visium Spatial Transcriptomic slides). a-h Expression of MSC subtype-specific transcripts, taken from the Phate analysis (average expression of the top 20 markers of each subtype, Supplementary Table 11). Expression of bone precursors on day 2 and 14 DPW ( a , b ). Expression of adipocyte precursors on day 2 and 14 DPW ( c , d ). Expression of bone/muscle precursors on day 2 and 14 DPW ( e , f ). Expression of fibroblast 2 on day 2 and 14 DPW ( g , h ). Expression of fibroblast 3 on day 2 and 14 DPW ( i , j ). 2 DPW represents inflammation stage (right column) and 14 DPW represents remodelling stage (left column) of wound healing. Scale bars: 500 um ( a - j ). The colour of the scales in a-j indicates the expression of transcripts mapped to the slide from low (blue) to high (red)

Journal: BMC Biology

Article Title: Transcriptomic characterization of transitioning cell types in the skin of Atlantic salmon

doi: 10.1186/s12915-025-02196-w

Figure Lengend Snippet: Charting the transcriptomic activity of different putative MSC-associated subclusters (10x Visium Spatial Transcriptomic slides). a-h Expression of MSC subtype-specific transcripts, taken from the Phate analysis (average expression of the top 20 markers of each subtype, Supplementary Table 11). Expression of bone precursors on day 2 and 14 DPW ( a , b ). Expression of adipocyte precursors on day 2 and 14 DPW ( c , d ). Expression of bone/muscle precursors on day 2 and 14 DPW ( e , f ). Expression of fibroblast 2 on day 2 and 14 DPW ( g , h ). Expression of fibroblast 3 on day 2 and 14 DPW ( i , j ). 2 DPW represents inflammation stage (right column) and 14 DPW represents remodelling stage (left column) of wound healing. Scale bars: 500 um ( a - j ). The colour of the scales in a-j indicates the expression of transcripts mapped to the slide from low (blue) to high (red)

Article Snippet: Fig. 5 Wound healing in Atlantic salmon. a Histological micrographs depicting incisional wound at 2 days post-wounding (DPW), with Alcian blue and periodic acid-Schiff (PAS) staining to facilitate viewing of the incisional wound during the inflammation stage b Histological micrographs depicting incisional wound at 14 DPW, with Movat staining to facilitate viewing of the granulation tissue during the remodelling stage. c - f 10x Visium Spatial Transcriptomics Slides.

Techniques: Activity Assay, Expressing

Cold fibrosis after MI is conserved in humans and in a clinically relevant porcine model (A and B) (A) Representative human left ventricle spatial transcriptomics slides (Visium) of patients following acute-myocardial infarction (MI) and non-transplanted donor hearts. Samples were divided based on time following MI as either: uninjured ( n = 10), early (days 0–15 post-MI; n = 6), and late (30 days+; n = 6). (B) Abundance of fibroblasts and myeloid cells was quantified based on deconvolution scores of cell types per spot . Myofibroblast were calculated as enrichment of the mean myofibroblast state score within spots with a minimal 10% value of cell-type abundance . Statistical analysis used Wilcoxon tests with Benjamini-Hochberg adjusted p values. (C) Experimental design of pig MI experiment: adult (3 months old) pigs underwent MI by temporarily occluding their LAD using a balloon catheter . Following reperfusion (balloon deflation), pigs were immediately treated with recombinant human Agrin (rhAgrin) or Saline control, in an antegrade trajectory. Injured pig hearts were collected at either day 3 ( n = 4 for rhAgrin; n = 3 for Saline) or day 28 ( n = 4 for rhAgrin; n = 3 for saline) and dissected to distinct tissue areas (infarct and remote zones). Remote and infarcted samples were subjected to bulk-mRNA sequencing and histology for fibrosis assessment. (D and E) Representative sirius red staining images are shown from (D) day 3 and (E) day 28 post-MI. Fibrosis was quantified as the average % fold change (FC) between infarct/remote zone sections for each pig individually. Fibrosis (day 3 or day 28) for Saline and rhAgrin hearts was measured using two-tailed unpaired t test. Scale bars: 1 mm. striated line denotes FC = 1. n.s, non-significant difference. (F and G) Heatmaps based on log 2 transformed normalized counts for all (upregulated and downregulated) differentially expressed genes (defined by |log 2 fold change| ≥ 1, p -adjusted value < 0.05 and max raw counts > 30) between remote and infarct zones for Saline and rhAgrin-treated hearts at day 3 (5,961 genes) (F) and 28 (1,079 genes) (G) post-MI. Rows represent genes and columns represent each biological sample and its spatial distribution according to infarct or remote zone. Data are represented as mean ± SD. (H) Hierarchical clustering per condition (day [3 or 28] +treatment [rhAgrin or Saline]), based on the 1,000 most variable genes. Triangles and circles represent remote and infarct zones, respectively. (I) Deconvolution of bulk-mRNA sequencing of pig hearts following MI of either rhAgrin (blue) or Saline-treated (red) samples. Macrophage and myofibroblast abundances were assessed by gene signatures as FC, between infarct and remote zones ( , C, and <xref ref-type=Table S5 ). (J) Macrophage and myofibroblast abundances, based on deconvolution of bulk-mRNA sequencing (as in I). Treated samples were compared per time point (day 3 or 28), separately by two-tailed unpaired Student t test. Results are represented as mean ± SEM. " width="100%" height="100%">

Journal: Cell Systems

Article Title: Cold and hot fibrosis define clinically distinct cardiac pathologies

doi: 10.1016/j.cels.2025.101198

Figure Lengend Snippet: Cold fibrosis after MI is conserved in humans and in a clinically relevant porcine model (A and B) (A) Representative human left ventricle spatial transcriptomics slides (Visium) of patients following acute-myocardial infarction (MI) and non-transplanted donor hearts. Samples were divided based on time following MI as either: uninjured ( n = 10), early (days 0–15 post-MI; n = 6), and late (30 days+; n = 6). (B) Abundance of fibroblasts and myeloid cells was quantified based on deconvolution scores of cell types per spot . Myofibroblast were calculated as enrichment of the mean myofibroblast state score within spots with a minimal 10% value of cell-type abundance . Statistical analysis used Wilcoxon tests with Benjamini-Hochberg adjusted p values. (C) Experimental design of pig MI experiment: adult (3 months old) pigs underwent MI by temporarily occluding their LAD using a balloon catheter . Following reperfusion (balloon deflation), pigs were immediately treated with recombinant human Agrin (rhAgrin) or Saline control, in an antegrade trajectory. Injured pig hearts were collected at either day 3 ( n = 4 for rhAgrin; n = 3 for Saline) or day 28 ( n = 4 for rhAgrin; n = 3 for saline) and dissected to distinct tissue areas (infarct and remote zones). Remote and infarcted samples were subjected to bulk-mRNA sequencing and histology for fibrosis assessment. (D and E) Representative sirius red staining images are shown from (D) day 3 and (E) day 28 post-MI. Fibrosis was quantified as the average % fold change (FC) between infarct/remote zone sections for each pig individually. Fibrosis (day 3 or day 28) for Saline and rhAgrin hearts was measured using two-tailed unpaired t test. Scale bars: 1 mm. striated line denotes FC = 1. n.s, non-significant difference. (F and G) Heatmaps based on log 2 transformed normalized counts for all (upregulated and downregulated) differentially expressed genes (defined by |log 2 fold change| ≥ 1, p -adjusted value < 0.05 and max raw counts > 30) between remote and infarct zones for Saline and rhAgrin-treated hearts at day 3 (5,961 genes) (F) and 28 (1,079 genes) (G) post-MI. Rows represent genes and columns represent each biological sample and its spatial distribution according to infarct or remote zone. Data are represented as mean ± SD. (H) Hierarchical clustering per condition (day [3 or 28] +treatment [rhAgrin or Saline]), based on the 1,000 most variable genes. Triangles and circles represent remote and infarct zones, respectively. (I) Deconvolution of bulk-mRNA sequencing of pig hearts following MI of either rhAgrin (blue) or Saline-treated (red) samples. Macrophage and myofibroblast abundances were assessed by gene signatures as FC, between infarct and remote zones ( , C, and Table S5 ). (J) Macrophage and myofibroblast abundances, based on deconvolution of bulk-mRNA sequencing (as in I). Treated samples were compared per time point (day 3 or 28), separately by two-tailed unpaired Student t test. Results are represented as mean ± SEM.

Article Snippet: Spatial transcriptomics slides (Visium 10X) of left ventricle tissues of patients with acute myocardial infarction and non-transplanted donor hearts were obtained from Kuppe et al. Labels provided by the original authors describing the distinct pathological zones and time-points after human myocardial infarction were used in the analyses.

Techniques: Recombinant, Saline, Control, Sequencing, Staining, Two Tailed Test, Transformation Assay

( A ) Violin plots showing expression of canonical marker genes in different endometrial cell types. ( B ) Violin plots showing PLA2G2A and DIO2 expression across different endometrial cell types with p -values based on Wilcoxon rank sum test; a.u., arbitrary units. ( C ) Column bar graphs depicting the relative abundance of stromal subsets across the indicated cycle days. ( D ) RNA velocity mapped onto UMAP plots of stromal subsets in nine endometrial biopsies. ( E ) Visualization of the GSEA hallmark ‘DNA Repair’ gene set in mid-luteal endometrium by Visium spatial transcriptomics (upper panel). The lower panel shows the corresponding tissue section stained with H&E.

Journal: bioRxiv

Article Title: Stalling of the endometrial decidual reaction determines the recurrence risk of miscarriage

doi: 10.1101/2024.11.07.622412

Figure Lengend Snippet: ( A ) Violin plots showing expression of canonical marker genes in different endometrial cell types. ( B ) Violin plots showing PLA2G2A and DIO2 expression across different endometrial cell types with p -values based on Wilcoxon rank sum test; a.u., arbitrary units. ( C ) Column bar graphs depicting the relative abundance of stromal subsets across the indicated cycle days. ( D ) RNA velocity mapped onto UMAP plots of stromal subsets in nine endometrial biopsies. ( E ) Visualization of the GSEA hallmark ‘DNA Repair’ gene set in mid-luteal endometrium by Visium spatial transcriptomics (upper panel). The lower panel shows the corresponding tissue section stained with H&E.

Article Snippet: Spaceranger software (version 1.3.0, 10x Genomics) was used to align and obtain raw counts from each of the spots on the Visium spatial transcriptomics slides against the GRCh38 human genome reference data (refdata-gex-GRCh38-2020-A).

Techniques: Expressing, Marker, Staining