ArticleJournal of molecular medicine (Berlin, Germany)2015
Smooth muscle 22α facilitates angiotensin II-induced signaling and vascular contraction.
Article in Journal of molecular medicine (Berlin, Germany), 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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Who cites it
14 citing papers in PubMed, 23 citations in OpenAlex.
- Human iPSC-EV-loaded nanofiber stent coatings accelerate vascular repair by enhancing EGFR/HIF-1α signaling and suppressing ROCK1-mediated remodeling.Materials today. Bio · 2026Article
- A novel glomerulopathy model demonstrates renal counterbalance via local angiotensin II regulation.Proceedings of the Japan Academy. Series B, Physical and biological sciences · 2025Article
- Dual-Specificity Phosphatase 6 Deficiency Attenuates Arterial-Injury-Induced Intimal Hyperplasia in Mice.International journal of molecular sciences · 2023Article
- Physiology and Proteomic Basis of Lung Adaptation to High-Altitude Hypoxia in Tibetan Sheep.Animals : an open access journal from MDPI · 2022Article
- PKN2 deficiency leads both to prenatal 'congenital' cardiomyopathy and defective angiotensin II stress responses.The Biochemical journal · 2022Article
- Inflammation and atherosclerosis: signaling pathways and therapeutic intervention.Signal transduction and targeted therapy · 2022Review
- Deletion of SM22α disrupts the structure and function of caveolae and T-tubules in cardiomyocytes, contributing to heart failure.PloS one · 2022Article
- Tripartite motif protein 11 (TRIM11), an oncogene for human lung cancer via the DUSP6-mediated ERK1/2 signaling pathway.Cancer biology & therapy · 2021Article
- DUSP6 SUMOylation protects cells from oxidative damage via direct regulation of Drp1 dephosphorylation.Science advances · 2020Article
- Integrative Genomics Analysis Unravels Tissue-Specific Pathways, Networks, and Key Regulators of Blood Pressure Regulation.Frontiers in cardiovascular medicine · 2019Article
- Immunoproteasome Inhibition Impairs T and B Cell Activation by Restraining ERK Signaling and Proteostasis.Frontiers in immunology · 2018Article
- Short-Term Angiotensin II Treatment Affects Large Artery Biomechanics and Function in the Absence of Small Artery Alterations in Mice.Frontiers in physiology · 2018Article
- Insulin-independent GLUT4 translocation in proliferative vascular smooth muscle cells involves SM22α.Journal of molecular medicine (Berlin, Germany) · 2017Article
- T3 inhibits the calcification of vascular smooth muscle cells and the potential mechanism.American journal of translational research · 2016Article
Corrections and comments
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Authors and funding
13 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
unlabelledSmooth muscle 22α (SM22α) is involved in stress fiber formation and enhances contractility in vascular smooth muscle cells (VSMCs). In many cases, SM22α acts as an adapter protein to assemble signaling complexes and regulate signaling, but whether SM22α regulates contractile signaling induced by angiotensin II (AngII) remains unclear. To address this issue, we established a hypertension model of Sm22α(-/-) mice, and demonstrated that hypertension induced by AngII was attenuated in Sm22α(-/-) mice. A decreased vasoconstriction was observed in aortic rings from Sm22α(-/-) mice. Furthermore, loss of SM22α resulted in a reduced contractile response to AngII in VSMCs in vitro. The phosphorylation of extracellular signal-regulated kinase 1/2 (ERK1/2) induced by AngII was impaired following depletion of SM22α, in parallel with a reduced contractility. The decay of ERK1/2 activity was associated with increased expression of mitogen-activated protein kinase phosphatase 3 (MKP3). Inhibition of MKP3 activity rescued ERK1/2 activity. SM22α depletion caused an enhanced interaction of MKP3 with ERK1/2, and a reduced ubiquitination and degradation of MKP3. Knockdown of SM22α extended the half-life of MKP3. In conclusion, SM22α promotes AngII-induced contraction by maintenance of ERK1/2 signaling cascades through facilitating ubiquitination and degradation of MKP3. KEY MESSAGE: The vasoconstriction is attenuated in aortic rings from Sm22α(-/-) mice. MKP3 mediates dephosphorylation of ERK1/2 in AngII-induced VSMC contraction. SM22α inhibits the interaction of ERK1/2 with MKP3. SM22α promotes ubiquitination and degradation of MKP3. SM22α facilitates AngII-induced contraction by maintenance of ERK1/2 signaling.
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