Inhibition of Fap Promotes Cardiac Repair by Stabilizing BNP

Inhibition of fibroblast activation protein promotes cardiac repair by stabilizing brain natriuretic peptide after myocardial infarction Bulk RNA-seq data of mouse cardiac fibroblasts (CFs) cultured alone in 3D GelMA hydrogel vs mouse CFs co-cultured with cardiac and lung endothelial cells in a ratio of 2:1 in 3D GelMA hydrogel. RNA-seq libraries from 3 biological replicates of mouse CFs cultured alone in 3D GelMA hydrogel vs mouse CFs co-cultured with cardiac and lung endothelial cells in a ratio of 2:1 in 3D GelMA hydrogel. Samples were subjected to paired-end sequencing by HiSeq XTen systems (Illumina, 150 bp reads). This study aims to test whether Fap is a critical regulator of cardiac repair after MI, and to uncover the underlying cellular and molecular mechanisms for better treatment of Myocardial infarction (MI). We then performed gene expression profiling analysis using data obtained from RNA-seq of 4 different tissues from sham, MI, FAPI (MI), FapKO (MI). Comparative gene expression profiling analysis of RNA-seq data for border zones of sham, MI, FAPI (MI), FapKO (MI).