https://transhumanist.ru/index.php?action=history&feed=atom&title=ADAM15 2026-08-28T19:15:58Z История изменений этой страницы в вики MediaWiki 1.43.6 https://transhumanist.ru/index.php?title=ADAM15&diff=5428&oldid=prev 2021-05-12T13:43:36Z

<p>Новая страница: «Disintegrin and metalloproteinase domain-containing protein 15 precursor (EC 3.4.24.-) (ADAM 15) (Metalloprotease RGD disintegrin protein) (Metalloproteinase-like...»</p> <p><b>Новая страница</b></p><div>Disintegrin and metalloproteinase domain-containing protein 15 precursor (EC 3.4.24.-) (ADAM 15) (Metalloprotease RGD disintegrin protein) (Metalloproteinase-like, disintegrin-like, and cysteine-rich protein 15) (MDC-15) (Metargidin) [MDC15]<br /> <br /> ==Publications==<br /> <br /> {{medline-entry<br /> |title=Homeostatic effects of the metalloproteinase disintegrin [[ADAM15]] in degenerative cartilage remodeling.<br /> |pubmed-url=https://pubmed.ncbi.nlm.nih.gov/15818704<br /> |abstract=The membrane-anchored metalloproteinase disintegrin [[ADAM15]] is up-regulated in osteoarthritis and has been implicated in proteolysis and cell-matrix interactions. To address its role in cartilage metabolism, we performed an analysis of joint morphology in aging mice with a targeted inactivation of the [[ADAM15]] gene ([[ADAM15]](-/-)). In addition, a human chondrocyte cell line overexpressing [[ADAM15]] was used to investigate the role of [[ADAM15]] in an in vitro model of chondrocyte-matrix interactions. Knee joint sections from 3-, 6-, and 12-14-month-old [[ADAM15]](-/-) and wild-type (WT) 129/SvJ mice were examined for synovial hyperplasia, cartilage degradation, and osteophyte formation. Stable transfection of the human T/C28a4 chondrocyte cell line with full-length human [[ADAM15]] complementary DNA led to the establishment of [[ADAM15]]-overexpressing chondrocytes that were further analyzed for their capability to adhere to and to survive on cartilage matrix molecules (fibronectin and types II and VI collagen) under conditions of serum starvation. [[ADAM15]] expression was investigated by reverse transcription-polymerase chain reaction and Western blotting. Aging [[ADAM15]](-/-) mice exhibited accelerated development of osteoarthritic lesions compared with WT mice, and the difference was statistically significant at age 12 months. The osteoarthritic changes preferentially affected male [[ADAM15]](-/-) mice. [[ADAM15]] overexpression in T/C28a4 cells led to the specific reinforcement of chondrocyte adhesion to cartilage types II and VI collagen, and this was associated with enhanced cell viability under conditions of serum starvation. The accelerated development of murine osteoarthritis in [[ADAM15]] deficiency as well as the proadhesive and cell survival-promoting in vitro effect of [[ADAM15]] overexpression suggest a homeostatic rather than a destructive role of [[ADAM15]] in cartilage remodeling.<br /> |mesh-terms=* ADAM Proteins<br /> * Aging<br /> * Animals<br /> * Blotting, Western<br /> * Cartilage, Articular<br /> * Cell Adhesion<br /> * Cell Line<br /> * Cell Survival<br /> * Chondrocytes<br /> * Disease Models, Animal<br /> * Female<br /> * Homeostasis<br /> * Humans<br /> * Male<br /> * Membrane Proteins<br /> * Metalloendopeptidases<br /> * Mice<br /> * Mice, Knockout<br /> * Osteoarthritis, Knee<br /> * RNA, Messenger<br /> * Reverse Transcriptase Polymerase Chain Reaction<br /> * Stifle<br /> * Synovial Membrane<br /> * Transfection<br /> <br /> |full-text-url=https://sci-hub.do/10.1002/art.20974<br /> }}</div>

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