دورية أكاديمية

Acute phase serum amyloid A induces proinflammatory cytokines and mineralization via toll-like receptor 4 in mesenchymal stem cells

التفاصيل البيبلوغرافية
العنوان: Acute phase serum amyloid A induces proinflammatory cytokines and mineralization via toll-like receptor 4 in mesenchymal stem cells
المؤلفون: Regina Ebert, Peggy Benisch, Melanie Krug, Sabine Zeck, Jutta Meißner-Weigl, Andre Steinert, Martina Rauner, Lorenz Hofbauer, Franz Jakob
المصدر: Stem Cell Research, Vol 15, Iss 1, Pp 231-239 (2015)
بيانات النشر: Elsevier, 2015.
سنة النشر: 2015
المجموعة: LCC:Biology (General)
مصطلحات موضوعية: Mesenchymal stem cells, Inflammation, Serum amyloid A, Toll-like receptor, Osteogenic differentiation, Mineralization, Biology (General), QH301-705.5
الوصف: The role of serum amyloid A (SAA) proteins, which are ligands for toll-like receptors, was analyzed in human bone marrow-derived mesenchymal stem cells (hMSCs) and their osteogenic offspring with a focus on senescence, differentiation and mineralization. In vitro aged hMSC developed a senescence-associated secretory phenotype (SASP), resulting in enhanced SAA1/2, TLR2/4 and proinflammatory cytokine (IL6, IL8, IL1β, CXCL1, CXCL2) expression before entering replicative senescence. Recombinant human SAA1 (rhSAA1) induced SASP-related genes and proteins in MSC, which could be abolished by cotreatment with the TLR4-inhibitor CLI-095. The same pattern of SASP-resembling genes was stimulated upon induction of osteogenic differentiation, which is accompanied by autocrine SAA1/2 expression. In this context additional rhSAA1 enhanced the SASP-like phenotype, accelerated the proinflammatory phase of osteogenic differentiation and enhanced mineralization. Autocrine/paracrine and rhSAA1 via TLR4 stimulate a proinflammatory phenotype that is both part of the early phase of osteogenic differentiation and the development of senescence. This signaling cascade is tightly involved in bone formation and mineralization, but may also propagate pathological extraosseous calcification conditions such as calcifying inflammation and atherosclerosis.
نوع الوثيقة: article
وصف الملف: electronic resource
اللغة: English
تدمد: 1873-5061
1876-7753
Relation: http://www.sciencedirect.com/science/article/pii/S1873506115000811; https://doaj.org/toc/1873-5061; https://doaj.org/toc/1876-7753
DOI: 10.1016/j.scr.2015.06.008
URL الوصول: https://doaj.org/article/8ca9f22dd7f14486ba38cb148069d19e
رقم الأكسشن: edsdoj.8ca9f22dd7f14486ba38cb148069d19e
قاعدة البيانات: Directory of Open Access Journals
الوصف
تدمد:18735061
18767753
DOI:10.1016/j.scr.2015.06.008