ArticleInternational journal of molecular sciences2020
The MEK/ERK Module Is Reprogrammed in Remodeling Adult Cardiomyocytes.
Article in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 16 citations in OpenAlex.
- Article
- DIRECTEUR: transcriptome-based prediction of small molecules that replace transcription factors for direct cell conversion.Bioinformatics (Oxford, England) · 2024Article
- Time-dependent effects of BRAF-V600E on cell cycling, metabolism, and function in engineered myocardium.Science advances · 2024Article
- Mechanistic insights into cardiac regeneration and protection through MEIS inhibition.Turkish journal of biology = Turk biyoloji dergisi · 2024Article
- Recent Perspectives on Cardiovascular Toxicity Associated with Colorectal Cancer Drug Therapy.Pharmaceuticals (Basel, Switzerland) · 2023Review
- MAPK-ERK Pathway.International journal of molecular sciences · 2023Article
- Risk prediction model construction for post myocardial infarction heart failure by blood immune B cells.Frontiers in immunology · 2023Article
- The Role of Oncostatin M and Its Receptor Complexes in Cardiomyocyte Protection, Regeneration, and Failure.International journal of molecular sciences · 2022Review
- Repression ofScience advances · 2021Article
- Myocardial Accumulations of Reg3A, Reg3γ and Oncostatin M Are Associated with the Formation of Granulomata in Patients with Cardiac Sarcoidosis.International journal of molecular sciences · 2021Article
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Authors and funding
12 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Fetal and hypertrophic remodeling are hallmarks of cardiac restructuring leading chronically to heart failure. Since the Ras/Raf/MEK/ERK cascade (MAPK) is involved in the development of heart failure, we hypothesized, first, that fetal remodeling is different from hypertrophy and, second, that remodeling of the MAPK occurs. To test our hypothesis, we analyzed models of cultured adult rat cardiomyocytes as well as investigated myocytes in the failing human myocardium by western blot and confocal microscopy. Fetal remodeling was induced through endothelial morphogens and monitored by the reexpression of Acta2, Actn1, and Actb. Serum-induced hypertrophy was determined by increased surface size and protein content of cardiomyocytes. Serum and morphogens caused reprogramming of Ras/Raf/MEK/ERK. In both models H-Ras, N-Ras, Rap2, B- and C-Raf, MEK1/2 as well as ERK1/2 increased while K-Ras was downregulated. Atrophy, MAPK-dependent ischemic resistance, loss of A-Raf, and reexpression of Rap1 and Erk3 highlighted fetal remodeling, while A-Raf accumulation marked hypertrophy. The knock-down of B-Raf by siRNA reduced MAPK activation and fetal reprogramming. In conclusion, we demonstrate that fetal and hypertrophic remodeling are independent processes and involve reprogramming of the MAPK.
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