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首页> 外文期刊>Journal of cellular physiology. >Novel insights into Dhh signaling in antler chondrocyte proliferation and differentiation: Involvement of Foxa
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Novel insights into Dhh signaling in antler chondrocyte proliferation and differentiation: Involvement of Foxa

机译：小说在鹿角洞察Dhh信号软骨细胞增殖和分化:参与Foxa

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摘要

The desert hedgehog (Dhh) is crucial for spermatogenesis and Leydig cell differentiation, but little is known regarding its physiological function in cartilage. In this study, Dhh mRNA was abundant in antler chondrocytes, where it advanced cell proliferation concomitant with accelerated transition from the G1 to the S phase and induced elevation of the hypertrophic chondrocyte markers, Col X and Runx2. Silencing of Ptch1 resulted in appreciable Smo accumulation and enhanced rDhh stimulation of Smo, whose impediment by cyclopamine obscured the proliferative function of Dhh and alleviated its guidance of chondrocyte differentiation. Further analysis evidenced the noteworthy positive action of Smo in the bridging between Dhh and Gli transcription factors. Obstruction of Gli1 by GANT58 caused the failed stimulation of Col X and Runx2 by rDhh. Analogously, siRNA against Gli1-3 hindered chondrocyte differentiation in the context of rDhh. Simultaneously, Gli transcription factors mediated the regulation of Dhh on Foxa1, Foxa2, and Foxa3, whose knockdown impaired chondrocyte differentiation. Attenuation of Foxa antagonized the augmentation of Col X and Runx2 generated by rDhh. Collectively, Dhh signaling through its target Foxa appears to induce antler chondrocyte proliferation and differentiation.
机译：沙漠刺猬(Dhh)是至关重要的精子发生和睾丸间质细胞分化,但有关它的生理所知甚少函数在软骨。在鹿茸软骨细胞丰富,它在哪里先进细胞增殖相伴加速过渡从G1 S期和诱导肥厚性的高度软骨细胞标记,X和Runx2坳。Ptch1导致明显的Smo的积累和增强rDhh Smo的刺激的环巴胺掩盖了障碍增生性Dhh并缓解其功能软骨细胞分化的指导。分析证明值得注意的积极行动Smo的桥接Dhh和Gli之间转录因子。GANT58导致失败的刺激坳X和Runx2 rDhh。阻碍了软骨细胞分化rDhh的上下文。转录因子介导的规定Dhh Foxa1, Foxa2 Foxa3,其可拆卸的受损的软骨细胞分化。的增加引起Foxa坳X和由rDhh Runx2生成。信号通过其目标Foxa似乎诱导鹿茸软骨细胞增殖分化。

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