کد مقاله کد نشریه سال انتشار مقاله انگلیسی نسخه تمام متن
5669269 1407954 2016 9 صفحه PDF دانلود رایگان
عنوان انگلیسی مقاله ISI
Unloading results in rapid loss of TGFβ signaling in articular cartilage: role of loading-induced TGFβ signaling in maintenance of articular chondrocyte phenotype?
موضوعات مرتبط
علوم پزشکی و سلامت پزشکی و دندانپزشکی ایمونولوژی، آلرژی و روماتولوژی
پیش نمایش صفحه اول مقاله
Unloading results in rapid loss of TGFβ signaling in articular cartilage: role of loading-induced TGFβ signaling in maintenance of articular chondrocyte phenotype?
چکیده انگلیسی

SummaryObjectiveRecently it was shown that loading of articular cartilage explants activates TGFβ signaling. Here we investigated if in vivo chondrocytes express permanently high TGFβ signaling, and the consequence of the loss of compressive loading-mediated TGFβ signaling on chondrocyte function and phenotype.MethodBovine articular cartilage explants were collected within 10 min post mortem and stained immediately and after 30, 60 and 360 min for phosphorylated-Smad2, indicating active TGFβ signaling. Explants were unloaded for 48 h and subsequently repeatedly loaded with a compressive load of 3 MPa. In addition, explants were cultured unloaded for 2 weeks and the effect of loading or exogenous TGFβ on proteoglycan level and chondrocyte phenotype (Col10a1 mRNA expression) was analyzed.ResultsUnloading of articular cartilage results in rapid loss of TGFβ signaling while subsequent compressive loading swiftly restored this. Loading and exogenous TGFβ enhanced expression of TGFβ1 and ALK5. Unloading of explants for 2 weeks resulted in proteoglycan loss and increased Col10a1 expression. Both loading and exogenous TGFβ inhibited elevated Col10a1 expression but not proteoglycan loss.ConclusionOur data might imply that in vivo regular physiological loading of articular cartilage leads to enduring TGFβ signaling and TGFβ-induced gene expression. We propose a hypothetical model in which loading activates a self-perpetuating system that prevents hypertrophic differentiation of chondrocytes and is crucial for cartilage homeostasis.

ناشر
Database: Elsevier - ScienceDirect (ساینس دایرکت)
Journal: Osteoarthritis and Cartilage - Volume 24, Issue 10, October 2016, Pages 1807-1815
نویسندگان
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