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Ellis-van Creveld syndrome protein homolog (Evc) was previously shown to mediate expression of Indian hedgehog (Ihh) downstream targets in chondrocytes. Consequently disruption of the Ihh/Pthrp axis was demonstrated in Evc−/− mice, but the full extent of Evc involvement in endochondral development was not totally characterized. Herein we have examined further the Evc−/− growth plate in a homogeneous genetic background and show that Evc promotes chondrocyte proliferation, chondrocyte hypertrophy and the differentiation of osteoblasts in the perichondrium, hence implicating Evc in both Pthrp-dependent and Pthrp-independent Ihh functions. We also demonstrate that Evc, which localizes to osteoblast primary cilia, mediates Hedgehog (Hh) signaling in the osteoblast lineage. In spite of this, bone collar development is mildly affected in Evc−/− mutants. The onset of perichondrial osteoblastogenesis is delayed at the initial stages of endochondral ossification in Evc−/− mice, and in later stages, the leading edge of expression of osteoblast markers and Wnt/β-catenin signaling components is located closer to the primary spongiosa in the Evc−/− perichondrium owing to impaired osteoblast differentiation. Additionally we have used Ptch1-LacZ reporter mice to learn about the different types of Hh-responsive cells that are present in the perichondrium of normal and Evc−/− mice. Evc mediates Hh target gene expression in inner perichondrial cells, but it is dispensable in the external layers of the perichondrium. Finally, we report cranial base defects in Evc−/− mice and reveal that Evc is essential for intrasphenoidal synchondrosis development.  相似文献
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王欢博  贺婷  郑超  卢玮光  范静  颉强  杨柳 《骨科》2021,12(6):485-492
目的 探究Indian Hedgehog(IHH)信号通路对软骨内成骨过程中软骨细胞成熟以及转分化的影响。方法 取10日龄野生型小鼠的胫骨组织,采用原位杂交和免疫组织化学染色检测生长板区域IHH信号通路相关分子IhhPtch1Gli1的表达水平。构建肥大软骨细胞特异性Ihh基因敲除小鼠(Col10a1Cre/+; Ihhnull/C),并采用影像学检查和阿利新蓝染色评估该小鼠的骨骼发育状况。构建肥大软骨细胞IHH信号通路持续激活小鼠(Col10a1Cre/+; R26SmoM2/M2Col10a1Cre/+; Ptch1LacZ/C),采用HE染色、原位杂交和TUNEL染色分别对受精15.5天胎鼠胫骨组织形态结构、Ihh(肥大软骨细胞分子标志物)和Col1a1(成骨细胞分子标志物)以及肥大软骨细胞凋亡水平进行检测;另外应用HE染色对10日龄小鼠的胫骨组织进行组织学分析。结果 肥大软骨细胞合成分泌IHH,但不表达Ptch1Gli1。抑制肥大软骨细胞合成IHH蛋白会导致出生后小鼠出现侏儒症;X线检查结果显示小鼠出现严重的骨骼发育不良,包括胸廓狭小、球形头骨以及椎骨发育异常等表现。持续启动IHH信号通路时,胚胎早期软骨细胞成熟分化过程虽未见异常,但是出生后小鼠的骨小梁、骨内膜以及皮质骨等结构均出现一定的异常表现。结论 IHH信号通路虽然不参与肥大软骨细胞的终末分化过程,但在软骨细胞转分化的过程中起到了重要的调控作用。  相似文献
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