ArticleFrontiers in cell and developmental biology2021
Myeloid MKL1 Disseminates Cues to Promote Cardiac Hypertrophy in Mice.
Article in Frontiers in cell and developmental biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed.
- An MRTF-A-ZEB1-IRF9 axis contributes to fibroblast-myofibroblast transition and renal fibrosis.Experimental & molecular medicine · 2023Article
- The heart under pressure: immune cells in fibrotic remodeling.Current opinion in physiology · 2022Article
- HES5-mediated repression of LIGHT transcription may contribute to apoptosis in hepatocytes.Cell death discovery · 2021Article
- Redox-sensitive activation of CCL7 by BRG1 in hepatocytes during liver injury.Redox biology · 2021Article
- Dual Regulation of Tank Binding Kinase 1 by BRG1 in Hepatocytes Contributes to Reactive Oxygen Species Production.Frontiers in cell and developmental biology · 2021Article
- A GSK3-SRF Axis Mediates Angiotensin II Induced Endothelin Transcription in Vascular Endothelial Cells.Frontiers in cell and developmental biology · 2021Article
- An E2F5-TFDP1-BRG1 Complex Mediates Transcriptional Activation of MYCN in Hepatocytes.Frontiers in cell and developmental biology · 2021Article
- Epigenetic Repression of Chloride Channel Accessory 2 Transcription in Cardiac Fibroblast: Implication in Cardiac Fibrosis.Frontiers in cell and developmental biology · 2021Article
- Resident Fibroblast MKL1 Is Sufficient to Drive Pro-fibrogenic Response in Mice.Frontiers in cell and developmental biology · 2021Article
- A KDM4-DBC1-SIRT1 Axis Contributes to TGF-b Induced Mesenchymal Transition of Intestinal Epithelial Cells.Frontiers in cell and developmental biology · 2021Article
- Choline Kinase Alpha Is a Novel Transcriptional Target of the Brg1 in Hepatocyte: Implication in Liver Regeneration.Frontiers in cell and developmental biology · 2021Article
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Authors and funding
8 authors.
Funding
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Abstract
Cardiac hypertrophy is a key pathophysiological process in the heart in response to stress cues. Although taking place in cardiomyocytes, the hypertrophic response is influenced by other cell types, both within the heart and derived from circulation. In the present study we investigated the myeloid-specific role of megakaryocytic leukemia 1 (MKL1) in cardiac hypertrophy. Following transverse aortic constriction (TAC), myeloid MKL1 conditional knockout (MFCKO) mice exhibit an attenuated phenotype of cardiac hypertrophy compared to the WT mice. In accordance, the MFCKO mice were protected from excessive cardiac inflammation and fibrosis as opposed to the WT mice. Conditioned media collected from macrophages enhanced the pro-hypertrophic response in cardiomyocytes exposed to endothelin in an MKL1-dependent manner. Of interest, expression levels of macrophage derived miR-155, known to promote cardiac hypertrophy, were down-regulated in the MFCKO mice compared to the WT mice. MKL1 depletion or inhibition repressed miR-155 expression in macrophages. Mechanistically, MKL1 interacted with NF-κB to activate miR-155 transcription in macrophages. In conclusion, our data suggest that MKL1 may contribute to pathological hypertrophy via regulating macrophage-derived miR-155 transcription.
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