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人软骨终板来源干细胞缺氧调节成骨分化过程中基因表达谱和可变剪接事件的全基因组分析。

A genome-wide analysis of the gene expression profiles and alternative splicing events during the hypoxia-regulated osteogenic differentiation of human cartilage endplate-derived stem cells.

作者信息

Yao Yuan, Deng Qiyue, Sun Chao, Song Weiling, Liu Huan, Zhou Yue

机构信息

Department of Orthopedics, Xinqiao Hospital, Third Military Medical University, Chongqing 400037, P.R. China.

Department of Neurobiology, College of Basic Medical Sciences, Third Military Medical University, Chongqing 400038, P.R. China.

出版信息

Mol Med Rep. 2017 Aug;16(2):1991-2001. doi: 10.3892/mmr.2017.6846. Epub 2017 Jun 22.

Abstract

It has been hypothesized that intervertebral disc degeneration is initiated by degeneration of the cartilage endplate (CEP), which is characterized by cartilage ossification. CEP‑derived stem cells (CESCs), with the potential for chondro‑osteogenic differentiation, may be responsible for the balance between chondrification and ossification in the CEP. The CEP remains in an avascular and hypoxic microenvironment; the present study observed that hypoxia was able to markedly inhibit the osteogenic differentiation of CESCs. This tissue‑specific CESC differentiation in response to a hypoxic microenvironment was physiologically important for the prevention of ossification in the CEP. In order to study the hypoxia‑regulated mechanisms underlying osteogenic differentiation of CESCs, a Human Transcriptome Array 2.0 was used to detect differentially expressed genes (DEGs) and alternatively spliced genes (ASGs) during the osteogenic differentiation of CESCs under hypoxia, compared with those induced under normoxia. High‑throughput analysis of DEGs and ASGs demonstrated that genes in the complement pathway were enriched, which may be a potential mechanism underlying hypoxia inhibition of CESCs osteogenesis. The results of the present study may provide a basis for future mechanistic studies regarding gene expression levels and alternative splicing events during the hypoxia‑regulated inhibition of osteogenesis, which may be helpful in identifying targets for CEP degeneration therapy.

摘要

据推测,椎间盘退变始于软骨终板(CEP)的退变,其特征为软骨骨化。具有软骨成骨分化潜能的CEP来源干细胞(CESCs)可能负责CEP中软骨化与骨化之间的平衡。CEP处于无血管且缺氧的微环境中;本研究观察到缺氧能够显著抑制CESCs的成骨分化。这种对缺氧微环境的组织特异性CESC分化对于预防CEP中的骨化具有重要生理意义。为了研究缺氧调节CESCs成骨分化的机制,使用人类转录组阵列2.0检测缺氧条件下CESCs成骨分化过程中与常氧诱导条件下相比的差异表达基因(DEGs)和可变剪接基因(ASGs)。对DEGs和ASGs的高通量分析表明补体途径中的基因富集,这可能是缺氧抑制CESCs成骨的潜在机制。本研究结果可为未来关于缺氧调节成骨抑制过程中基因表达水平和可变剪接事件的机制研究提供基础,这可能有助于确定CEP退变治疗的靶点。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8089/5562021/5ebca688dbe7/MMR-16-02-1991-g00.jpg

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