Datasets

Title	Myocardial cellular gene expression during pressure overload: evidence for transient partial endothelial to mesenchymal transition [Ribo-seq]
Organism
Number of Samples	9
Release Date	2021/07/23 00:00
Sequencing Types
Protocol Details

Title
Authors	Froese N,Cordero J,Abouissa A,Trogisch FA,Grein S,Szaroszyk M,Wang Y,Gigina A,Korf-Klingebiel M,Bosnjak B,Davenport CF,Wiehlmann L,Geffers R,Riechert E,Jürgensen L,Boileau E,Lin Y,Dieterich C,Förster R,Bauersachs J,Ola R,Dobreva G,Völkers M,Heineke J
Journal	iScience
Publication Date	2022 Mar 18
Abstract	To identify cellular mechanisms responsible for pressure overload triggered heart failure, we isolated cardiomyocytes, endothelial cells, and fibroblasts as most abundant cell types from mouse hearts in the subacute and chronic stages after transverse aortic constriction (TAC) and performed RNA-sequencing. We detected highly cell-type specific transcriptional responses with characteristic time courses and active intercellular communication. Cardiomyocytes after TAC exerted an early and sustained upregulation of inflammatory and matrix genes and a concomitant suppression of metabolic and ion channel genes. Fibroblasts, in contrast, showed transient early upregulation of inflammatory and matrix genes and downregulation of angiogenesis genes, but sustained induction of cell cycle and ion channel genes during TAC. Endothelial cells transiently induced cell cycle and extracellular matrix genes early after TAC, but exerted a long-lasting upregulation of inflammatory genes. As we found that matrix production by multiple cell types triggers pathological cellular responses, it might serve as a future therapeutic target. © 2022 The Author(s).
PMC	PMC8908217
PMID	35281736
DOI

Froese et al. 2022 (PRJNA749295)