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Role and regulation of growth plate vascularization during coupling with osteogenesis in tibial dyschondroplasia of chickens

机译:生长板血管化与成骨作用在鸡胫骨软骨发育不良中的作用和调节

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Tibial dyschondroplasia (TD) is the most-prevalent leg disorder in fast-growing chickens; it is intractable and characterized by abnormal endochondral bone formation of proximal tibial growth-plates (TGPs). Previous studies have shown that bone is a highly vascularized tissue dependent on the coordinated coupling between angiogenesis and osteogenesis, but the underlying mechanisms of bone formation and bone remodeling are poorly defined in TD chickens. Here, we observed that inhibition of vasculogenesis and angiogenesis remarkably impaired vascular invasion in the hypertrophic chondrocyte zone of the TGPs, resulting in the massive death of chondrocytes due to a shortage of blood vessels and nutrients. Moreover, the balance of the OPG (osteoprotegerin)/RANKL (receptor activator of nuclear factor-kB ligand) system is also severely disrupted during the osteogenesis process while coupling with angiogenesis, both of which eventually lead to abnormal endochondral bone formation in TD chickens. Thus, the process of vascular formation in endochondral bone appears to initiate the pathological changes in TD, and improvement of this process during coupling with osteogenesis may be a potential therapeutic approach to treat this intractable disease.
机译:胫骨软骨发育不良(TD)是快速生长的鸡中最普遍的腿部疾病。它是顽固的,其特征是胫骨近端生长板(TGPs)的软骨内骨形成异常。先前的研究表明,骨骼是高度血管化的组织,取决于血管生成和成骨之间的协调耦合,但是在TD鸡中,骨骼形成和骨骼重塑的基本机制尚不明确。在这里,我们观察到血管生成和血管生成的抑制显着损害了TGPs肥大软骨细胞区域中的血管入侵,由于血管和营养物质的缺乏,导致软骨细胞大量死亡。此外,在成骨过程中同时与血管生成耦合的同时,OPG(骨保护素)/ RANKL(核因子-kB配体的受体激活剂)系统的平衡也被严重破坏,这两者最终都会导致TD鸡的软骨内骨形成异常。因此,软骨内骨中血管形成的过程似乎引发了TD的病理变化,并且在与成骨过程相结合的过程中改善这一过程可能是治疗这种顽固性疾病的潜在治疗方法。

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