Artikel ; Online: TRPC6 regulates phenotypic switching of vascular smooth muscle cells through plasma membrane potential-dependent coupling with PTEN.
2019 Band 33, Heft 9, Seite(n) 9785–9796
Abstract: Vascular smooth muscle cells (VSMCs) play critical roles in the stability and tonic regulation ... facilitated contractile differentiation of VSMCs through plasma membrane hyperpolarization. TRPC6-deficient ... phenotypic switching of VSMCs is a hallmark of vascular disorders such as atherosclerosis and restenosis ...
| Abstract | Vascular smooth muscle cells (VSMCs) play critical roles in the stability and tonic regulation of vascular homeostasis. VSMCs can switch back and forth between highly proliferative synthetic and fully differentiated contractile phenotypes in response to changes in the vessel environment. Although abnormal phenotypic switching of VSMCs is a hallmark of vascular disorders such as atherosclerosis and restenosis after angioplasty, how control of VSMC phenotypic switching is dysregulated in pathologic conditions remains obscure. We found that inhibition of canonical transient receptor potential 6 (TRPC6) channels facilitated contractile differentiation of VSMCs through plasma membrane hyperpolarization. TRPC6-deficient VSMCs exhibited more polarized resting membrane potentials and higher protein kinase B (Akt) activity than wild-type VSMCs in response to TGF-β1 stimulation. Ischemic stress elicited by oxygen-glucose deprivation suppressed TGF-β1-induced hyperpolarization and VSMC differentiation, but this effect was abolished by TRPC6 deletion. TRPC6-mediated Ca |
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| Mesh-Begriff(e) | Animals ; Aorta ; Cell Line ; Cell Membrane ; Membrane Potentials/physiology ; Mice ; Muscle, Smooth, Vascular/cytology ; Myocytes, Smooth Muscle/metabolism ; PTEN Phosphohydrolase/genetics ; PTEN Phosphohydrolase/metabolism ; Proto-Oncogene Proteins c-akt/metabolism ; TRPC6 Cation Channel/genetics ; TRPC6 Cation Channel/metabolism | ||||||||||
| Chemische Substanzen | TRPC6 Cation Channel ; Trpc6 protein, mouse ; Proto-Oncogene Proteins c-akt (EC 2.7.11.1) ; PTEN Phosphohydrolase (EC 3.1.3.67) ; Pten protein, mouse (EC 3.1.3.67) | ||||||||||
| Sprache | Englisch | ||||||||||
| Erscheinungsdatum | 2019-06-04 | ||||||||||
| Erscheinungsland | United States | ||||||||||
| Dokumenttyp | Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't | ||||||||||
| ZDB-ID | 639186-2 | ||||||||||
| ISSN | 1530-6860 ; 0892-6638 | ||||||||||
| ISSN (online) | 1530-6860 | ||||||||||
| ISSN | 0892-6638 | ||||||||||
| DOI | 10.1096/fj.201802811R | ||||||||||
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| Datenquelle | MEDical Literature Analysis and Retrieval System OnLINE |
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