دورية أكاديمية
أعرض في EDS

Abnormal mechanosensing and cofilin activation promote the progression of ascending aortic aneurysms in mice.

التفاصيل البيبلوغرافية
العنوان: Abnormal mechanosensing and cofilin activation promote the progression of ascending aortic aneurysms in mice.
المؤلفون: Yamashiro Y; Department of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA., Papke CL; Department of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA., Kim J; Department of Mechanical Engineering and Materials Science, Washington University, St. Louis, MO 63130, USA., Ringuette LJ; Department of Anatomy and Cell Biology, McGill University, Montreal, Quebec H3A 0C7, Canada., Zhang QJ; Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA., Liu ZP; Department of Internal Medicine, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA., Mirzaei H; Department of Biochemistry and Proteomics Core Unit, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA., Wagenseil JE; Department of Mechanical Engineering and Materials Science, Washington University, St. Louis, MO 63130, USA., Davis EC; Department of Anatomy and Cell Biology, McGill University, Montreal, Quebec H3A 0C7, Canada., Yanagisawa H; Department of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA. Life Science Center of Tsukuba Advanced Research Alliance, University of Tsukuba, Tsukuba 305-8577, Japan. hkyanagisawa@tara.tsukuba.ac.jp.
المصدر: Science signaling [Sci Signal] 2015 Oct 20; Vol. 8 (399), pp. ra105. Date of Electronic Publication: 2015 Oct 20.
نوع المنشور: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
اللغة: English
بيانات الدورية: Publisher: American Association for the Advancement of Science Country of Publication: United States NLM ID: 101465400 Publication Model: Electronic Cited Medium: Internet ISSN: 1937-9145 (Electronic) Linking ISSN: 19450877 NLM ISO Abbreviation: Sci Signal Subsets: MEDLINE
أسماء مطبوعة: Original Publication: Washington, D.C. : American Association for the Advancement of Science
مواضيع طبية MeSH: Actin Depolymerizing Factors/*physiology , Aortic Aneurysm/*physiopathology, Animals ; Disease Progression ; Mice
مستخلص: Smooth muscle cells (SMCs) and the extracellular matrix (ECM) are intimately associated in the aortic wall. Fbln4(SMKO) mice with an SMC-specific deletion of the Fbln4 gene, which encodes the vascular ECM component fibulin-4, develop ascending aortic aneurysms that have increased abundance of angiotensin-converting enzyme (ACE); inhibiting angiotensin II signaling within the first month of life prevents aneurysm development. We used comparative proteomics analysis of Fbln4(SMKO) aortas from postnatal day (P) 1 to P30 mice to identify key molecules involved in aneurysm initiation and expansion. At P14, the actin depolymerizing factor cofilin was dephosphorylated and thus activated, and at P7, the abundance of slingshot-1 (SSH1) phosphatase, an activator of cofilin, was increased, leading to actin cytoskeletal remodeling. Also, by P7, biomechanical changes and underdeveloped elastic lamina-SMC connections were evident, and the abundance of early growth response 1 (Egr1), a mechanosensitive transcription factor that stimulates ACE expression, was increased, which was before the increases in ACE abundance and cofilin activation. Postnatal deletion of Fbln4 in SMCs at P7 prevented cofilin activation and aneurysm formation, suggesting that these processes required disruption of elastic lamina-SMC connections. Phosphoinositide 3-kinase (PI3K) is involved in the angiotensin II-mediated activation of SSH1, and administration of PI3K inhibitors from P7 to P30 decreased SSH1 abundance and prevented aneurysms. These results suggest that aneurysm formation arises from abnormal mechanosensing of SMCs resulting from the loss of elastic lamina-SMC connections and from increased SSH1 and cofilin activity, which may be potential therapeutic targets for treating ascending aortic aneurysms.
(Copyright © 2015, American Association for the Advancement of Science.)
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معلومات مُعتمدة: R01 HL105314 United States HL NHLBI NIH HHS; R01 HL106305 United States HL NHLBI NIH HHS; R01HL106305 United States HL NHLBI NIH HHS; R01 HL115560 United States HL NHLBI NIH HHS; R01 HL085749 United States HL NHLBI NIH HHS; T32 HL007360 United States HL NHLBI NIH HHS; F32 HL122076-01 United States HL NHLBI NIH HHS; 5T32HL007360-34 United States HL NHLBI NIH HHS; F32 HL122076 United States HL NHLBI NIH HHS; R01HL115560 United States HL NHLBI NIH HHS
المشرفين على المادة: 0 (Actin Depolymerizing Factors)
تواريخ الأحداث: Date Created: 20151022 Date Completed: 20160801 Latest Revision: 20181113
رمز التحديث: 20240628
مُعرف محوري في PubMed: PMC5572214
DOI: 10.1126/scisignal.aab3141
PMID: 26486174
قاعدة البيانات: MEDLINE
الوصف
تدمد:1937-9145
DOI:10.1126/scisignal.aab3141