يعرض 1 - 10 نتائج من 91 نتيجة بحث عن '"cartilage matrix degradation"', وقت الاستعلام: 1.00s تنقيح النتائج
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    دورية أكاديمية

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    دورية أكاديمية

    المصدر: European Cells & Materials, Vol 30, Pp 200-209 (2012)

    مصطلحات موضوعية: which promote chondrocyte apoptosis and degrade cartilage to potentiate PTOA development. Recent studies show that the rate-limiting step for transcriptional activation of injury response genes is controlled by cyclin-dependent kinase 9 (CDK9), and thus it is an attractive target for limiting the injury response. Here, we determined the effects of CDK9 inhibition in suppressing the injury response in mechanically-injured cartilage explants. Bovine cartilage explants were injured by a single compressive load of 30 % strain at 100 %/s, and then treated with the CDK9 inhibitor Flavopiridol. To assess acute injury responses, we measured the mRNA expression of pro-inflammatory cytokines, catabolic enzymes, and apoptotic genes by RT-PCR, and chondrocyte viability and apoptosis by TUNEL staining. For long-term outcome, cartilage matrix degradation was assessed by soluble glycosaminoglycan release, and by determining the mechanical properties with instantaneous and relaxation moduli. Our data showed CDK9 inhibitor markedly reduced injury-induced inflammatory cytokine and catabolic gene expression. CDK9 inhibitor also attenuated chondrocyte apoptosis and reduced cartilage matrix degradation. Lastly, the mechanical properties of the injured explants were preserved by CDK9 inhibitor. Our results provide a temporal profile connecting the chain of events from mechanical impact, acute injury responses, to the subsequent induction of chondrocyte apoptosis and cartilage matrix deterioration. Thus, CDK9, Flavopiridol, inflammatory cytokines, chondrocytes, Diseases of the musculoskeletal system, RC925-935, Orthopedic surgery, RD701-811

    وصف الملف: electronic resource

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    كتاب إلكتروني

    المساهمون: Beck, F., editorAff1, Clascá, F., editorAff2, Frotscher, M., editorAff3, Haines, D. E., editorAff4, Hirokawa, N., editorAff5, Kmiec, Z., editorAff6, Korf, H. -W., editorAff7, Marani, E., editorAff8, Putz, R., editorAff9, Sano, Y., editorAff10, Schiebler, T. H., editorAff11, Timmermans, J. -P., editorAff12, Mobasheri, AliAff13, Bondy, Carolyn A.Aff14, Moley, KelleAff15, Mendes, Alexandrina FerreiraAff16, Rosa, Susana CarvalhoAff16, Richardson, Stephen M.Aff17, Hoyland, Judith A.Aff17, Barrett-Jolley, RichardAff18, Shakibaei, MehdiAff19

    المصدر: Facilitative Glucose Transporters in Articular Chondrocytes : Expression, Distribution and Functional Regulation of GLUT Isoforms by Hypoxia, Hypoxia Mimetics, Growth Factors and Pro-Inflammatory Cytokines. 200:50-53

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    دورية أكاديمية

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    كتاب إلكتروني

    المؤلفون: Lark, Michael W.Aff3, Bayne, Ellen K.Aff4, Lohmander, L. StefanAff5

    المساهمون: Parnham, Michael J., editorAff1, Bottomley, Kevin M. K., editorAff2, Bradshaw, David, editorAff2, Nixon, John S., editorAff2

    المصدر: Metalloproteinases as Targets for Anti-Inflammatory Drugs. :59-83

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