Редактирование: EFNB2

Ephrin-B2 precursor (EPH-related receptor tyrosine kinase ligand 5) (LERK-5) (HTK ligand) (HTK-L) [EPLG5] [HTKL] [LERK5]

==Publications==

{{medline-entry
|title=Cartilage-specific deletion of ephrin-B2 in mice results in early developmental defects and an osteoarthritis-like phenotype during aging in vivo.
|pubmed-url=https://pubmed.ncbi.nlm.nih.gov/26980243
|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.
|mesh-terms=* Aging
* Animals
* Arthritis, Experimental
* Bone Development
* Cartilage, Articular
* Ephrin-B2
* Immunohistochemistry
* Mice
* Mice, Knockout
* Mice, Transgenic
* Osteoarthritis
* Phenotype
* X-Ray Microtomography
|keywords=* Bone development
* Ephrin-B2
* Knockout mouse model
* Osteoarthritis
|full-text-url=https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4791873
}}