دورية أكاديمية
أعرض في EDS

Smooth muscle hyperplasia due to loss of smooth muscle α-actin is driven by activation of focal adhesion kinase, altered p53 localization and increased levels of platelet-derived growth factor receptor-β.

التفاصيل البيبلوغرافية
العنوان: Smooth muscle hyperplasia due to loss of smooth muscle α-actin is driven by activation of focal adhesion kinase, altered p53 localization and increased levels of platelet-derived growth factor receptor-β.
المؤلفون: Papke CL; Department of Internal Medicine, University of Texas Health Science Center at Houston, 6431 Fannin, MSB 6.100, Houston, TX 77030, USA., Cao J, Kwartler CS, Villamizar C, Byanova KL, Lim SM, Sreenivasappa H, Fischer G, Pham J, Rees M, Wang M, Chaponnier C, Gabbiani G, Khakoo AY, Chandra J, Trache A, Zimmer W, Milewicz DM
المصدر: Human molecular genetics [Hum Mol Genet] 2013 Aug 01; Vol. 22 (15), pp. 3123-37. Date of Electronic Publication: 2013 Apr 15.
نوع المنشور: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
اللغة: English
بيانات الدورية: Publisher: IRL Press at Oxford University Press Country of Publication: England NLM ID: 9208958 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1460-2083 (Electronic) Linking ISSN: 09646906 NLM ISO Abbreviation: Hum Mol Genet Subsets: MEDLINE
أسماء مطبوعة: Original Publication: Oxford, England ; New York : IRL Press at Oxford University Press, c1992-
مواضيع طبية MeSH: Actins/*metabolism , Focal Adhesion Protein-Tyrosine Kinases/*metabolism , Myocytes, Smooth Muscle/*metabolism , Myocytes, Smooth Muscle/*pathology , Receptor, Platelet-Derived Growth Factor beta/*metabolism , Tumor Suppressor Protein p53/*metabolism, Actins/genetics ; Animals ; Cell Movement/genetics ; Cell Nucleus/metabolism ; Cell Proliferation ; Enzyme Activation ; Hyperplasia ; Mice ; Mice, Knockout ; Models, Biological ; Phenotype ; Protein Transport ; Reactive Oxygen Species/metabolism
مستخلص: Mutations in ACTA2, encoding the smooth muscle cell (SMC)-specific isoform of α-actin (α-SMA), cause thoracic aortic aneurysms and dissections and occlusive vascular diseases, including early onset coronary artery disease and stroke. We have shown that occlusive arterial lesions in patients with heterozygous ACTA2 missense mutations show increased numbers of medial or neointimal SMCs. The contribution of SMC hyperplasia to these vascular diseases and the pathways responsible for linking disruption of α-SMA filaments to hyperplasia are unknown. Here, we show that the loss of Acta2 in mice recapitulates the SMC hyperplasia observed in ACTA2 mutant SMCs and determine the cellular pathways responsible for SMC hyperplasia. Acta2(-/-) mice showed increased neointimal formation following vascular injury in vivo, and SMCs explanted from these mice demonstrated increased proliferation and migration. Loss of α-SMA induced hyperplasia through focal adhesion (FA) rearrangement, FA kinase activation, re-localization of p53 from the nucleus to the cytoplasm and increased expression and ligand-independent activation of platelet-derived growth factor receptor beta (Pdgfr-β). Disruption of α-SMA in wild-type SMCs also induced similar cellular changes. Imatinib mesylate inhibited Pdgfr-β activation and Acta2(-/-) SMC proliferation in vitro and neointimal formation with vascular injury in vivo. Loss of α-SMA leads to SMC hyperplasia in vivo and in vitro through a mechanism involving FAK, p53 and Pdgfr-β, supporting the hypothesis that SMC hyperplasia contributes to occlusive lesions in patients with ACTA2 missense mutations.
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معلومات مُعتمدة: P01 HL110869 United States HL NHLBI NIH HHS; P50HL083794-01 United States HL NHLBI NIH HHS; R01 HL62594 United States HL NHLBI NIH HHS; UL1 RR024148 United States RR NCRR NIH HHS
المشرفين على المادة: 0 (Actins)
0 (Reactive Oxygen Species)
0 (Tumor Suppressor Protein p53)
EC 2.7.10.1 (Receptor, Platelet-Derived Growth Factor beta)
EC 2.7.10.2 (Focal Adhesion Protein-Tyrosine Kinases)
تواريخ الأحداث: Date Created: 20130418 Date Completed: 20140131 Latest Revision: 20221109
رمز التحديث: 20221213
مُعرف محوري في PubMed: PMC3699068
DOI: 10.1093/hmg/ddt167
PMID: 23591991
قاعدة البيانات: MEDLINE
الوصف
تدمد:1460-2083
DOI:10.1093/hmg/ddt167