ArticlePloS one2015
Myocardin Family Members Drive Formation of Caveolae.
Article in PloS one, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 42 citations in OpenAlex.
- MAPK14 converges on key transcriptional machinery to promote vascular smooth muscle cell degeneration in abdominal aortic aneurysm.Signal transduction and targeted therapy · 2026Article
- Hippo in smooth muscle - a therapeutic target in vascular diseases driven by aging and hypertension.Frontiers in physiology · 2025Review
- Suppression of smooth muscle cell inflammation by myocardin-related transcription factors involves inactivation of TANK-binding kinase 1.Scientific reports · 2024Article
- Vascular smooth muscle-specific YAP/TAZ deletion triggers aneurysm development in mouse aorta.JCI insight · 2023Article
- YAP and TAZ in Vascular Smooth Muscle Confer Protection Against Hypertensive Vasculopathy.Arteriosclerosis, thrombosis, and vascular biology · 2022Article
- Endothelial Transcytosis in Acute Lung Injury: Emerging Mechanisms and Therapeutic Approaches.Frontiers in physiology · 2022Review
- MRTF may be the missing link in a multiscale mechanobiology approach toward macrophage dysfunction in space.Frontiers in cell and developmental biology · 2022Article
- NG2/CSPG4, CD146/MCAM and VAP1/AOC3 are regulated by myocardin-related transcription factors in smooth muscle cells.Scientific reports · 2021Article
- Cell Type Dependent Suppression of Inflammatory Mediators by Myocardin Related Transcription Factors.Frontiers in physiology · 2021Article
- Regulation of the Muscarinic MFrontiers in physiology · 2021Article
- Caveolin1 Tyrosine-14 Phosphorylation: Role in Cellular Responsiveness to Mechanical Cues.The Journal of membrane biology · 2020Review
- The Hippo Pathway Regulates Caveolae Expression and Mediates Flow Response via Caveolae.Current biology : CB · 2019Article
- Nexilin/NEXN controls actin polymerization in smooth muscle and is regulated by myocardin family coactivators and YAP.Scientific reports · 2018Article
- Myocyte membrane and microdomain modifications in diabetes: determinants of ischemic tolerance and cardioprotection.Cardiovascular diabetology · 2017Review
- Injury induced expression of caveolar proteins in human kidney tubules - role of megakaryoblastic leukemia 1.BMC nephrology · 2017Article
- Cavin-3 (PRKCDBP) deficiency reduces the density of caveolae in smooth muscle.Cell and tissue research · 2017Article
- Hypertension reduces soluble guanylyl cyclase expression in the mouse aorta via the Notch signaling pathway.Scientific reports · 2017Article
- Similar regulatory mechanisms of caveolins and cavins by myocardin family coactivators in arterial and bladder smooth muscle.PloS one · 2017Article
- Rosiglitazone drives cavin-2/SDPR expression in adipocytes in a CEBPα-dependent manner.PloS one · 2017Article
- Emerging roles of the myocardin family of proteins in lipid and glucose metabolism.The Journal of physiology · 2016Review
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Authors and funding
12 authors at 2 institutions in 2 countries.
Funding
Abstract
Caveolae are membrane organelles that play roles in glucose and lipid metabolism and in vascular function. Formation of caveolae requires caveolins and cavins. The make-up of caveolae and their density is considered to reflect cell-specific transcriptional control mechanisms for caveolins and cavins, but knowledge regarding regulation of caveolae genes is incomplete. Myocardin (MYOCD) and its relative MRTF-A (MKL1) are transcriptional coactivators that control genes which promote smooth muscle differentiation. MRTF-A communicates changes in actin polymerization to nuclear gene transcription. Here we tested if myocardin family proteins control biogenesis of caveolae via activation of caveolin and cavin transcription. Using human coronary artery smooth muscle cells we found that jasplakinolide and latrunculin B (LatB), substances that promote and inhibit actin polymerization, increased and decreased protein levels of caveolins and cavins, respectively. The effect of LatB was associated with reduced mRNA levels for these genes and this was replicated by the MRTF inhibitor CCG-1423 which was non-additive with LatB. Overexpression of myocardin and MRTF-A caused 5-10-fold induction of caveolins whereas cavin-1 and cavin-2 were induced 2-3-fold. PACSIN2 also increased, establishing positive regulation of caveolae genes from three families. Full regulation of CAV1 was retained in its proximal promoter. Knock down of the serum response factor (SRF), which mediates many of the effects of myocardin, decreased cavin-1 but increased caveolin-1 and -2 mRNAs. Viral transduction of myocardin increased the density of caveolae 5-fold in vitro. A decrease of CAV1 was observed concomitant with a decrease of the smooth muscle marker calponin in aortic aneurysms from mice (C57Bl/6) infused with angiotensin II. Human expression data disclosed correlations of MYOCD with CAV1 in a majority of human tissues and in the heart, correlation with MKL2 (MRTF-B) was observed. The myocardin family of transcriptional coactivators therefore drives formation of caveolae and this effect is largely independent of SRF.
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