Gene expression of cardiac fibroblasts post-MI
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PROVIDER: PRJNA435730 | ENA |
REPOSITORIES: ENA
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Project description:Cardiac fibroblasts stay relatively quiescent under normal condition. These cells differentiate to myofibroblasts after myocardial infarction (MI), characterized by the expression of contractile proteins and secretion of elevated levels of extracellular matrix proteins, leading to cardiac remodeling. The differentiated myofiroblasts gradually lose most myofibroblast phenotypes but still persist in the infarct area to maintain the tissue structural integrity. We used microarrays to reveal the change in cardiac fibroblast gene expression profile after MI.
2018-02-24 | GSE111059 | GEO
Project description:Analysis of one-day cultured cardiac fibroblasts after acute myocardial infarction
2020-05-20 | MSV000085454 | MassIVE
Project description:Cardiac fibrosis is a common feature of ischemic heart disease and cardiac fibroblasts (CF) are key players in cardiac remodeling of the injured heart after myocardial infarction (MI). Fibrosis increases myocardial stiffness, thereby impairing cardiac function, which ultimately progresses to end-stage heart failure. Little is known, however, on the secretome of CF and cell-to-cell communication of CF is only incompletely understood. Here, we in vivo labeled secreted proteins by expressing TurboID under control of the POSTN promotor in cardiac fibroblasts of mouse with myocardial infarction, enriched biotinylated proteins and analyzed them using LC-MS.
2025-03-25 | PXD053791 | Pride
Project description:Heart failure (HF) is a leading cause of morbidity and mortality. As adult cardiomyocytes (CMs) have little regenerative capacity, after myocardial infarction (MI), resident cardiac fibroblasts (CFs) synthesize extracellular matrix to form scar tissues, resulting in myocardial remodeling and HF. Thus, both cardiac regeneration and fibrosis are therapeutic targets for chronic MI. We previously reported that fibroblasts were directly reprogrammed into induced CMs (iCMs) by overexpression of cardiogenic transcription factors in acute and chronic MI. Here we show that in vivo cardiac reprogramming improved cardiac function, and reversed cardiac remodeling in chronic MI using a novel transgenic mouse system. Transcriptome analysis revealed that in vivo cardiac reprogramming suppressed signs of fibrosis and inflammation. Thus, in vivo cardiac reprogramming may be a promising approach for chronic HF.
2024-07-01 | GSE240310 | GEO
Project description:In response to myocardial infarction (MI), quiescent cardiac fibroblasts differentiate into myofibroblasts mediating tissue repair in the infarcted area. One of the most widely accepted markers of myofibroblast differentiation is the expression of Acta2 which encodes smooth muscle alpha-actin (SMαA) that is assembled into stress fibers. However, the requirement of Acta2/ SMαA in the myofibroblast differentiation of cardiac fibroblasts and its role in post-MI cardiac repair remained largely unknown. To answer these questions, we generated a tamoxifen-inducible cardiac fibroblast-specific Acta2 knockout mouse line. Surprisingly, mice that lacked Acta2 in cardiac fibroblasts had a normal survival rate after MI. Moreover, Acta2 deletion did not affect the function or overall histology of infarcted hearts. No difference was detected in the proliferation, migration, or contractility between WT and Acta2-null cardiac myofibroblasts. It was identified that Acta2-null cardiac myofibroblasts had a normal total filamentous actin level and total actin level. Acta2 deletion caused a significant compensatory increase in the transcription level of non- Acta2 actin isoforms, especially Actg2 and Acta1, 2 other muscle actin isoforms. Moreover, in myofibroblasts the transcription levels of cytoplasmic actin isoforms were significantly higher than those of muscle actin isoforms. In addition, we found that myocardin-related transcription factor-A is critical for myofibroblast differentiation but is not required for the compensatory effects of non-Acta2 isoforms. In conclusion, the deletion of Acta2 does not prevent the myofibroblast differentiation of cardiac fibroblasts or affect the post-MI cardiac repair, and the increased expression and stress fiber formation of non-SMαA actin isoforms and the functional redundancy between actin isoforms are able to compensate for the loss of Acta2 in cardiac myofibroblasts.
2022-01-10 | GSE193163 | GEO
Project description:Signal-induced proliferation-associated gene 1 (Sipa1) is known as a specific Rap1 GTPase-activating protein that negatively regulates Rap1 signaling. Although Sipa1 has been extensively studied in cancer research, its role in the wound healing response after myocardial infarction (MI) remains unexplored. To investigate the role of endogenous Sipa1 in MI, we performed permanent left anterior descending artery ligation in both Sipa1 knockout mice and their control littermates. Bone marrow transplantation, flow cytometry, cell sorting, and transcriptomic analysis were conducted to identify the cellular source of Sipa1 in the infarcted heart. The role of cardiac fibroblast-derived Sipa1 during MI was examined using Sipa1 deletion approaches, specifically in cardiac fibroblasts, in vivo and in vitro. Mice deficient in Sipa1 exhibited improved post-MI survival and cardiac function, along with attenuated expression of inflammatory mediators and diminished accumulation of Ly6Chigh monocytes and CCR2+ macrophages in the infarcted heart. Although Sipa1 was broadly expressed in the heart, cardiac fibroblasts were responsible for the Sipa1-induced deleterious phenotype as demonstrated by cardiac fibroblast-specific Sipa1 conditional knockout mice, which averted excessive inflammation and adverse cardiac remodeling following MI. Mechanistically, Sipa1 promotes the production of CCL2, CCL7 and granulocyte/macrophage colony-stimulating factor in the cardiac fibroblasts early after MI via a non-canonical RasGRP2-Ras-JNK signaling pathway, irrespective of canonical Rap1, thereby facilitating the accumulation and activation of inflammatory monocytes and macrophages. These results identify a previously unknown fibroblast-immune axis characterized by Sipa1, which initiates excessive inflammation and leads to poor outcomes after MI. Targeting Sipa1 offers a potential novel therapeutic strategy to optimize post-MI wound healing response, thereby preventing the development of chronic ischemic heart failure.
2025-08-01 | GSE295755 | GEO
Project description:Immune cell infiltration in response to myocyte death contributes to extracellular matrix (ECM) remodeling and scar formation after myocardial infarction (MI). Caspase-recruitment domain protein 9 (CARD9) which belongs to CARD family acts as an adapter that mediate the transduction of proinflammatory signaling cascades in innate immunity. To investigate the role of CARD9 in cardiac injury and repair post ischemia, we subjected Card9 knockout mice to myocardial infarction (MI) , and then performed RNA-seq and gene expression profiling analysis using the ischemic cardiac tissues at 3 days post-MI, to identify key genes and pathways regulated by CARD9.
2023-10-25 | GSE235257 | GEO
Project description:1-day and 7-day sham and MI hearts Keywords = Heart Keywords = Mycardial infarction Keywords = 1 day post-MI Keywords = 7 day post-MI Keywords: parallel sample
2005-11-10 | GSE1957 | GEO
Project description:In this study, we used a cardiac-specific, inducible expression system to activate YAP in adult mouse heart. Activation of YAP in adult heart promoted cardiomyocyte proliferation and did not deleteriously affect heart function. Furthermore, YAP activation after myocardial infarction (MI) preserved heart function and reduced infarct size. Using adeno-associated virus subtype 9 (AAV9) as a delivery vector, we expressed human YAP in the murine myocardium immediately after MI. We found that AAV9:hYAP significantly improved cardiac function and mouse survival. AAV9:hYAP did not exert its salutary effects by reducing cardiomyocyte apoptosis. Rather, we found that AAV9:hYAP stimulated adult cardiomyocyte proliferation. Gene expression profiling indicated that AAV9:hYAP stimulated cell cycle gene expression, enhanced TGFβ-signaling, and activated of components of the inflammatory response.Cardiac specific YAP activation after MI mitigated myocardial injury after MI, improved cardiac function and mouse survival. These findings suggest that therapeutic activation of hYAP or its downstream targets, potentially through AAV-mediated gene therapy, may be a strategy to improve outcome after MI. Three groups were involved in this study: sham group, AAV9:Luci+MI group and AAV9-YAP+MI group. Each group contained three biological replicates. The sham group had neither myocardial infarction nor AAV injection. The AAV9:Luci +MI(L for brief) group had myocardial infarction and injected with AAV9:Luic. The AAV9:hYAP+MI(YAP for brief) group had myocardial infarction and injected with AAV9:hYAP. 5 days after MI and AAV injection, the heart apexes were collected and the total RNA were isolated for microarray analysis.
2014-05-26 | E-GEOD-54612 | biostudies-arrayexpress
Project description:The molecular mechanism underlying cardiac remodeling following myocardial infarction have been incompletely understood. Until now, most studies have been performed in rodents. We studied cardiac remodeling in the physiologically more relevant animal model, the swine. Microarray analysis was performed on animals that underwent either sham surgery or permanent ligation of the left coronary artery (MI). RNA was isolated from the remote, non-ischemic, regions of the left ventricle. RNA was isolated from 8 sham and 8 MI animals three weeks after surgery. Each group contained 4 males and 4 females. Animals used for the study were 2-3 months old Yorkshire x Landrace swine. Only neutered males entered the study.
2011-12-21 | E-GEOD-27962 | biostudies-arrayexpress