human cardiac fibroblast cells  (PromoCell)

Journal: CytoJournal

Article Title: Transglutaminase 2 inhibition ameliorates cardiac fibrosis in myocardial infarction by inducing M2 macrophage polarization in vitro and in vivo

doi: 10.25259/Cytojournal_32_2024

Figure Lengend Snippet: Transglutaminase 2 downregulation transforming growth factor (TGF)-β1-induced myocardial fibrosis and repressed TGF-β1/small mother against decapentaplegic 3 (Smad3) pathway in mouse cardiac fibroblasts. (a and b) Small interfering negative control (si-NC) and siTransglutaminase 2 (si-TG2) were transfected to mouse cardiac fibroblasts isolated from C57BL/6 mice, and the protein expression of TG2 was detected through Western blot. (c-f) Mouse cardiac fibroblasts were treated with 100 µg/mL TGF-β1 to induce fibrosis, followed by transfection with siNC and si-TG2 for 48 h. Western blot was conducted to determine the levels of fibrosis-associated proteins, including collagen I, collagen III, and α-smooth muscle actin (α-SMA), in mouse cardiac fibroblasts after TGF-β1 treatment and transfection ( n = 3). (g-i) Western blot was also used in the assessment of the levels of TGF-β1, phospho-Smad3 (p-Smad3), and Smad3 in mouse cardiac fibroblasts after TGF-β1 treatment and transfection ( n = 3). (* P < 0.05. GAPDH: Glyceraldehyde-3-phosphate dehydrogenase.)

Article Snippet: The in vitro experiments involved the stimulation of cardiac fibroblasts with 100 µg/mL TGF-β1 (7754-BH, R and D Systems, Minneapolis, MN, USA) for 24 h to construct a myocardial fibrosis model. Next, the effects of knocking down TG2 on fibrosis were assessed using a myocardial fibrosis cell model. IL-4 (10 ng/mL, 404-ML; R and D Systems, Minneapolis, MN, USA) was used to interfere with bone marrow-derived macrophages (BMDMs) for 24 h to induce macrophage polarization.

Techniques: Negative Control, Transfection, Isolation, Expressing, Western Blot

Journal: bioRxiv

Article Title: Dissecting Regulatory Non-Coding Heart Disease GWAS Loci with High-Resolution 3D Chromatin Interactions Reveals Causal Genes with Pathophysiological Relevance to Heart Failure

doi: 10.1101/2024.10.08.617295

Figure Lengend Snippet: Bulk RNA-seq of HCM, NHCFV, and iHCF cells. A) Pearson correlation coefficients of transcriptome-wide expression levels in HCM, NHCFV, and iHCF. B) Heatmap of expression levels (log 2 (FPKQ+1) of cardiomyocyte marker genes and cardiac fibroblast marker genes in cell types used in this study.

Article Snippet: Specifically, we cultured 50 million primary Human Cardiac Myocytes (HCM) cells as well as Normal Human Cardiac Fibroblasts – Ventricular (NHCFV) primary cells, which are commercially available from PromoCell and Lonza respectively.

Techniques: RNA Sequencing Assay, Expressing, Marker

Journal: bioRxiv

Article Title: Dissecting Regulatory Non-Coding Heart Disease GWAS Loci with High-Resolution 3D Chromatin Interactions Reveals Causal Genes with Pathophysiological Relevance to Heart Failure

doi: 10.1101/2024.10.08.617295

Figure Lengend Snippet: Tracing regulatory circuits from GWAS signals to target genes using functional genomics. (A) Graphical summary of analyses annotating GWAS loci with 3D chromatin interaction and open chromatin data to prioritize functional variants and identify target genes that may underlie disease associations. Significant eQTLs further corroborated these SNP-gene relationships. (B) Analysis workflow for integration of genetic, expression, and functional genomic data. We layered significant pairwise interactions (chromatin loops) with SNPs and TSSs filtered for accessible regions and highlighted those in expressed TFs’ footprints and expressed target genes, as well as GTEx eQTLs, to identify putative active and functional SNP-gene pairs. (C) Genome-wide contact maps of high-resolution Hi-C interactions from primary human cardiac myocytes (HCM) and normal human cardiac fibroblasts –ventricular (NHCFV) (D) Number of GWAS SNPs associated with heart disease-related traits, including heart failure.

Article Snippet: Specifically, we cultured 50 million primary Human Cardiac Myocytes (HCM) cells as well as Normal Human Cardiac Fibroblasts – Ventricular (NHCFV) primary cells, which are commercially available from PromoCell and Lonza respectively.

Techniques: Functional Assay, Expressing, Genome Wide, Hi-C

Journal: bioRxiv

Article Title: Dissecting Regulatory Non-Coding Heart Disease GWAS Loci with High-Resolution 3D Chromatin Interactions Reveals Causal Genes with Pathophysiological Relevance to Heart Failure

doi: 10.1101/2024.10.08.617295

Figure Lengend Snippet: Prioritization of active and functional heart disease-associated SNP-gene pairs in human cardiac myocytes (HCM) and normal human cardiac fibroblasts – ventricular (NHCFV) combining genetics, epigenetics, and transcriptomics. A) Sankey diagram of the cell type-specific variation observed in heart disease-associated SNPs and gene accessibility after filtering for open chromatin, chromatin interaction, and expression features, as outlined in . B) Quantification of accessible SNPs identified in HCM and NHCFV that are within known transcription factor (TF) footprints of TFs that also have detectable mRNA expression. C) Number and overlap of active and functional SNP-gene pairs and corresponding unique target genes identified by GOTHiC and HICCUPS across HCM and NHCFV cells.

Article Snippet: Specifically, we cultured 50 million primary Human Cardiac Myocytes (HCM) cells as well as Normal Human Cardiac Fibroblasts – Ventricular (NHCFV) primary cells, which are commercially available from PromoCell and Lonza respectively.

Techniques: Functional Assay, Expressing