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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). Figure created in BioRender, and is licensed under CC BY 4.0 ( https://biorender.com/r54nzgf ). Sample size: n = 2 ECM hydrogel replicates, 7658 spots. b Myocardium (green) was labeled with anti-alpha-actinin antibody alongside fluorescently tagged ECM hydrogel (light blue) with nuclei stained with DAPI (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 downregulated 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. Significance was determined via nonparametric Wilcoxon rank-sum tests with a Benjamini–Hochberg FDR adjustment to determine gene lists ( d ), and via Kolmogoro-Smirnov tests and permutation testing, with Benjamin-Hochberg FDR adjustment ( e , f ). Source data are provided as a Source Data file. ECM extracellular matrix, Neg negative, reg regulation, Pop population, Prolif proliferation, FC fold change.
10x Visium Spatial Transcriptomics Slide, supplied by Spatial Transcriptomics Inc, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
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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). Figure created in BioRender, and is licensed under CC BY 4.0 ( https://biorender.com/r54nzgf ). Sample size: n = 2 ECM hydrogel replicates, 7658 spots. b Myocardium (green) was labeled with anti-alpha-actinin antibody alongside fluorescently tagged ECM hydrogel (light blue) with nuclei stained with DAPI (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 downregulated 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. Significance was determined via nonparametric Wilcoxon rank-sum tests with a Benjamini–Hochberg FDR adjustment to determine gene lists ( d ), and via Kolmogoro-Smirnov tests and permutation testing, with Benjamin-Hochberg FDR adjustment ( e , f ). Source data are provided as a Source Data file. ECM extracellular matrix, Neg negative, reg regulation, Pop population, Prolif proliferation, FC fold change.

Journal: Nature Communications

Article Title: Regional and cell specific bioactivity of injectable extracellular matrix biomaterials in myocardial infarction

doi: 10.1038/s41467-025-65351-5

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). Figure created in BioRender, and is licensed under CC BY 4.0 ( https://biorender.com/r54nzgf ). Sample size: n = 2 ECM hydrogel replicates, 7658 spots. b Myocardium (green) was labeled with anti-alpha-actinin antibody alongside fluorescently tagged ECM hydrogel (light blue) with nuclei stained with DAPI (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 downregulated 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. Significance was determined via nonparametric Wilcoxon rank-sum tests with a Benjamini–Hochberg FDR adjustment to determine gene lists ( d ), and via Kolmogoro-Smirnov tests and permutation testing, with Benjamin-Hochberg FDR adjustment ( e , f ). Source data are provided as a Source Data file. ECM extracellular matrix, Neg negative, reg regulation, Pop population, Prolif proliferation, FC fold change.

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, Labeling, Staining

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. Figure created in BioRender, and is licensed under CC BY 4.0 ( https://biorender.com/r54nzgf ). Sample size: n = 3 ECM hydrogel replicates, 9594 spots. b Myocardium (green) was labeled 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. Significance was determined via nonparametric Wilcoxon rank-sum tests with a Benjamini–Hochberg FDR adjustment to determine gene lists ( d ), and via Kolmogoro–Smirnov tests and permutation testing, with Benjamin–Hochberg FDR adjustment ( e, f ). Source data are provided as a Source Data file. ECM extracellular matrix, Neg negative, reg regulation, Pop population, Prolif proliferation, FC fold change.

Journal: Nature Communications

Article Title: Regional and cell specific bioactivity of injectable extracellular matrix biomaterials in myocardial infarction

doi: 10.1038/s41467-025-65351-5

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. Figure created in BioRender, and is licensed under CC BY 4.0 ( https://biorender.com/r54nzgf ). Sample size: n = 3 ECM hydrogel replicates, 9594 spots. b Myocardium (green) was labeled 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. Significance was determined via nonparametric Wilcoxon rank-sum tests with a Benjamini–Hochberg FDR adjustment to determine gene lists ( d ), and via Kolmogoro–Smirnov tests and permutation testing, with Benjamin–Hochberg FDR adjustment ( e, f ). Source data are provided as a Source Data file. ECM extracellular matrix, Neg negative, reg regulation, Pop population, Prolif proliferation, FC fold change.

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, Labeling, 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. Significance was determined via nonparametric Wilcoxon rank-sum tests with a Benjamini–Hochberg FDR adjustment to determine gene lists ( a, c – f ), and via Kolmogorov–Smirnov tests and permutation testing, with Benjamini–Hochberg FDR adjustment ( c – f ). Source data are provided as a Source Data file. ECM extracellular matrix, neg negative, vasc vascular, pos positive, reg regulation, pop population, prolif proliferation.

Journal: Nature Communications

Article Title: Regional and cell specific bioactivity of injectable extracellular matrix biomaterials in myocardial infarction

doi: 10.1038/s41467-025-65351-5

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. Significance was determined via nonparametric Wilcoxon rank-sum tests with a Benjamini–Hochberg FDR adjustment to determine gene lists ( a, c – f ), and via Kolmogorov–Smirnov tests and permutation testing, with Benjamini–Hochberg FDR adjustment ( c – f ). Source data are provided as a Source Data file. ECM extracellular matrix, neg negative, vasc vascular, pos positive, reg regulation, pop population, prolif proliferation.

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