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Ihh下调对软骨细胞生长和分化的抑制作用。

The inhibitory roles of Ihh downregulation on chondrocyte growth and differentiation.

作者信息

Deng Ang, Zhang Hongqi, Hu Minyu, Liu Shaohua, Wang Yuxiang, Gao Qile, Guo Chaofeng

机构信息

Department of Spine Surgery, Xiangya Hospital of Central South University, Changsha, Hunan 410008, P.R. China.

Department of Nutrition and Food Hygiene, School of Public Health, Central South University, Changsha, Hunan 410078, P.R. China.

出版信息

Exp Ther Med. 2018 Jan;15(1):789-794. doi: 10.3892/etm.2017.5458. Epub 2017 Nov 7.

DOI:10.3892/etm.2017.5458
PMID:29434683
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5772930/
Abstract

The proliferative rate of chondrocytes affects bone elongation. Chondrocyte hypertrophy is required for endochondral bone formation as chondrocytes secrete factors required for osteoblast differentiation and maturation. Previous studies have demonstrated that the Indian hedgehog (Ihh) signaling pathway is a key regulator of skeletal development and homeostasis. The aim of the present study was to investigate the function of Ihh in chondrocyte proliferation and differentiation, as well as the underlying mechanisms. Ihh was knocked down in mouse chondrocyte cells using short hairpin RNA. Chondrocyte apoptosis and cell cycle arrest were assessed using flow cytometry and the results indicated that knockdown of Ihh significantly inhibited cell growth (P<0.05) and increased apoptosis (P<0.001) compared with negative control cells. Downregulation of Ihh also resulted in cell cycle arrest at G1 to S phase in chondrocytes. It was also observed that knockdown of Ihh decreased alkaline phosphatase activity and mineral deposition of chondrocytes. The inhibitory roles of Ihh downregulation on chondrocyte growth and differentiation may be associated with the transforming growth factor-β/mothers against decapentaplegic and osteoprotegerin/receptor activator of nuclear factor κB ligand signaling pathway. The results of the present study suggest that chondrocyte-derived Ihh is essential for maintaining bone growth plates and that manipulation of Ihh expression or its signaling components may be a novel therapeutic technique for the treatment of skeletal diseases, including achondroplasia.

摘要

软骨细胞的增殖速率影响骨骼生长。软骨内骨形成需要软骨细胞肥大，因为软骨细胞分泌成骨细胞分化和成熟所需的因子。先前的研究表明，印度刺猬因子（Ihh）信号通路是骨骼发育和稳态的关键调节因子。本研究的目的是探讨Ihh在软骨细胞增殖和分化中的作用及其潜在机制。使用短发夹RNA在小鼠软骨细胞中敲低Ihh。使用流式细胞术评估软骨细胞凋亡和细胞周期阻滞，结果表明，与阴性对照细胞相比，敲低Ihh显著抑制细胞生长（P<0.05）并增加凋亡（P<0.001）。Ihh的下调还导致软骨细胞在G1期至S期的细胞周期阻滞。还观察到敲低Ihh会降低软骨细胞的碱性磷酸酶活性和矿物质沉积。Ihh下调对软骨细胞生长和分化的抑制作用可能与转化生长因子-β/抗五聚体蛋白母系和骨保护素/核因子κB受体激活剂配体信号通路有关。本研究结果表明，软骨细胞来源的Ihh对于维持骨生长板至关重要，并且操纵Ihh表达或其信号成分可能是治疗包括软骨发育不全在内的骨骼疾病的一种新型治疗技术。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/14e6/5772930/0a3666f7166b/etm-15-01-0789-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/14e6/5772930/0b339f97c4d7/etm-15-01-0789-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/14e6/5772930/e306c904044b/etm-15-01-0789-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/14e6/5772930/30252488d573/etm-15-01-0789-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/14e6/5772930/be46c48c9aba/etm-15-01-0789-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/14e6/5772930/0a3666f7166b/etm-15-01-0789-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/14e6/5772930/0b339f97c4d7/etm-15-01-0789-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/14e6/5772930/e306c904044b/etm-15-01-0789-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/14e6/5772930/30252488d573/etm-15-01-0789-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/14e6/5772930/be46c48c9aba/etm-15-01-0789-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/14e6/5772930/0a3666f7166b/etm-15-01-0789-g04.jpg

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