دورية أكاديمية
أعرض في EDS

Decreased pericellular matrix production and selection for enhanced cell membrane repair may impair osteocyte responses to mechanical loading in the aging skeleton.

التفاصيل البيبلوغرافية
العنوان: Decreased pericellular matrix production and selection for enhanced cell membrane repair may impair osteocyte responses to mechanical loading in the aging skeleton.
المؤلفون: Hagan ML; Department of Cellular Biology and Anatomy, Medical College of Georgia, Augusta University, Augusta, GA., Yu K; Department of Cellular Biology and Anatomy, Medical College of Georgia, Augusta University, Augusta, GA., Zhu J; Department of Cellular Biology and Anatomy, Medical College of Georgia, Augusta University, Augusta, GA., Vinson BN; Department of Cellular Biology and Anatomy, Medical College of Georgia, Augusta University, Augusta, GA., Roberts RL; Department of Cellular Biology and Anatomy, Medical College of Georgia, Augusta University, Augusta, GA., Montesinos Cartagena M; Department of Cellular Biology and Anatomy, Medical College of Georgia, Augusta University, Augusta, GA., Johnson MH; Department of Neuroscience and Regenerative Medicine, Augusta University, Augusta, GA., Wang L; Department of Mechanical Engineering, University of Delaware, Newark, DE., Isales CM; Department of Neuroscience and Regenerative Medicine, Augusta University, Augusta, GA., Hamrick MW; Department of Cellular Biology and Anatomy, Medical College of Georgia, Augusta University, Augusta, GA., McNeil PL; Department of Cellular Biology and Anatomy, Medical College of Georgia, Augusta University, Augusta, GA., McGee-Lawrence ME; Department of Cellular Biology and Anatomy, Medical College of Georgia, Augusta University, Augusta, GA.; Department of Orthopaedic Surgery, Augusta University, Augusta, GA.
المصدر: Aging cell [Aging Cell] 2020 Jan; Vol. 19 (1), pp. e13056. Date of Electronic Publication: 2019 Nov 19.
نوع المنشور: Journal Article; Research Support, N.I.H., Extramural; Research Support, U.S. Gov't, Non-P.H.S.
اللغة: English
بيانات الدورية: Publisher: Wiley-Blackwell Country of Publication: England NLM ID: 101130839 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1474-9726 (Electronic) Linking ISSN: 14749718 NLM ISO Abbreviation: Aging Cell Subsets: MEDLINE
أسماء مطبوعة: Publication: Oxford, UK : Wiley-Blackwell
Original Publication: Oxford, UK : Blackwell Pub., c2002-
مواضيع طبية MeSH: Cell Membrane/*metabolism , Mechanotransduction, Cellular/*physiology , Osteocytes/*metabolism, Aging ; Animals ; Female ; Humans ; Male ; Mice
مستخلص: Transient plasma membrane disruptions (PMD) occur in osteocytes with in vitro and in vivo loading, initiating mechanotransduction. The goal here was to determine whether osteocyte PMD formation or repair is affected by aging. Osteocytes from old (24 months) mice developed fewer PMD (-76% females, -54% males) from fluid shear than young (3 months) mice, and old mice developed fewer osteocyte PMD (-51%) during treadmill running. This was due at least in part to decreased pericellular matrix production, as studies revealed that pericellular matrix is integral to formation of osteocyte PMD, and aged osteocytes produced less pericellular matrix (-55%). Surprisingly, osteocyte PMD repair rate was faster (+25% females, +26% males) in osteocytes from old mice, and calcium wave propagation to adjacent nonwounded osteocytes was blunted, consistent with impaired mechanotransduction downstream of PMD in osteocytes with fast PMD repair in previous studies. Inducing PMD via fluid flow in young osteocytes in the presence of oxidative stress decreased postwounding cell survival and promoted accelerated PMD repair in surviving cells, suggesting selective loss of slower-repairing osteocytes. Therefore, as oxidative stress increases during aging, slower-repairing osteocytes may be unable to successfully repair PMD, leading to slower-repairing osteocyte death in favor of faster-repairing osteocyte survival. Since PMD are an important initiator of mechanotransduction, age-related decreases in pericellular matrix and loss of slower-repairing osteocytes may impair the ability of bone to properly respond to mechanical loading with bone formation. These data suggest that PMD formation and repair mechanisms represent new targets for improving bone mechanosensitivity with aging.
(© 2019 The Authors. Aging Cell published by the Anatomical Society and John Wiley & Sons Ltd.)
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معلومات مُعتمدة: P01 AG036675 United States AG NIA NIH HHS; P01-AG036675 United States AG NIA NIH HHS
فهرسة مساهمة: Keywords: aging; bone; mechanical loading; mechanotransduction; osteocyte; skeleton
تواريخ الأحداث: Date Created: 20191120 Date Completed: 20210113 Latest Revision: 20240214
رمز التحديث: 20240214
مُعرف محوري في PubMed: PMC6974724
DOI: 10.1111/acel.13056
PMID: 31743583
قاعدة البيانات: MEDLINE
الوصف
تدمد:1474-9726
DOI:10.1111/acel.13056