https://transhumanist.ru/index.php?action=history&feed=atom&title=EFNB2 2026-04-14T05:18:42Z История изменений этой страницы в вики MediaWiki 1.43.6 https://transhumanist.ru/index.php?title=EFNB2&diff=6456&oldid=prev 2021-05-12T15:31:29Z

<p>Новая страница: «Ephrin-B2 precursor (EPH-related receptor tyrosine kinase ligand 5) (LERK-5) (HTK ligand) (HTK-L) [EPLG5] [HTKL] [LERK5] ==Publications== {{medline-entry |title...»</p> <p><b>Новая страница</b></p><div>Ephrin-B2 precursor (EPH-related receptor tyrosine kinase ligand 5) (LERK-5) (HTK ligand) (HTK-L) [EPLG5] [HTKL] [LERK5]<br /> <br /> ==Publications==<br /> <br /> {{medline-entry<br /> |title=Cartilage-specific deletion of ephrin-B2 in mice results in early developmental defects and an osteoarthritis-like phenotype during aging in vivo.<br /> |pubmed-url=https://pubmed.ncbi.nlm.nih.gov/26980243<br /> |abstract=Ephrins and their related receptors have been implicated in some developmental events. We have demonstrated that ephrin-B2 ([[EFNB2]]) could play a role in knee joint pathology associated with osteoarthritis (OA). Here, we delineate the in vivo role of [[EFNB2]] in musculoskeletal growth, development, and in OA using a cartilage-specific [[EFNB2]] knockout ([[EFNB2]](Col2)KO) mouse model. [[EFNB2]](Col2)KO was generated with Col2a1-Cre transgenic mice. The skeletal development was evaluated using macroscopy, immunohistochemistry, histomorphometry, radiology, densitometry, and micro-computed tomography. Analyses were performed at P0 (birth) and on postnatal days P15, P21, and on 8-week- and 1-year-old mice. [[EFNB2]](Col2)KO mice exhibited significant reduction in size, weight, length, and in long bones. At P0, the growth plates of [[EFNB2]](Col2)KO mice displayed increased type X collagen, disorganized hyphertrophic zone, and decreased mineralization. At P15, mutant mice demonstrated a significant reduction in VEGF and TRAP at the chondro-osseous junction and a delay in the secondary ossification, including a decrease in bone volume and trabecular thickness. At P21 and 8 weeks old, [[EFNB2]](Col2)KO mice exhibited reduced bone mineral density in the total skeleton, femur and spine. One-year-old [[EFNB2]](Col2)KO mice demonstrated OA phenotypic features in both the knee and hip. By P15, 27 % of the [[EFNB2]](Col2)KO mice developed a hip locomotor phenotype, which further experiments demonstrated reflected the neurological midline abnormality involving the corticospinal tract. This in vivo study demonstrated, for the first time, that [[EFNB2]] is essential for normal long bone growth and development and its absence leads to a knee and hip OA phenotype in aged mice.<br /> |mesh-terms=* Aging<br /> * Animals<br /> * Arthritis, Experimental<br /> * Bone Development<br /> * Cartilage, Articular<br /> * Ephrin-B2<br /> * Immunohistochemistry<br /> * Mice<br /> * Mice, Knockout<br /> * Mice, Transgenic<br /> * Osteoarthritis<br /> * Phenotype<br /> * X-Ray Microtomography<br /> |keywords=* Bone development<br /> * Ephrin-B2<br /> * Knockout mouse model<br /> * Osteoarthritis<br /> |full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4791873<br /> }}</div>

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