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Beclin 1 过表达抑制骨关节炎软骨细胞凋亡并下调细胞外基质代谢。

Beclin 1 overexpression inhibits chondrocyte apoptosis and downregulates extracellular matrix metabolism in osteoarthritis.

机构信息

Department of Internal Medicine, Guizhou Osteological Hospital, Guiyang, Guizhou 550007, P.R. China.

Department of Pathology, Guizhou Osteological Hospital, Guiyang, Guizhou 550007, P.R. China.

出版信息

Mol Med Rep. 2017 Oct;16(4):3958-3964. doi: 10.3892/mmr.2017.7064. Epub 2017 Jul 21.

DOI:10.3892/mmr.2017.7064
PMID:28731147
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5646975/
Abstract

In the present study, the expression of Beclin 1 in osteoarthritis (OA) cartilage tissue was investigated, and also its role in proliferation, apoptosis and expression of matrix metalloproteinases (MMPs) in chondrocytes obtained from patients with OA. Beclin 1 expression in cartilage tissue from OA patients, and in the age- and sex-matched controls, was detected by immunohistochemistry, semi-quantitative polymerase chain reaction and western blotting. Chondrocytes were divided into control and Beclin 1-overexpressed groups. After transfection for 48, 72 and 96 h, cell viability, apoptosis, the phosphatidylinositol-3-kinase (PI3K)/protein kinase B (Akt)/mammalian target of rapamycin (mTOR) signaling pathway and MMPs were examined. The mRNA and protein expression levels of Beclin 1 were significantly decreased in cartilage tissue from OA patients compared with the sex- and age-matched controls (P<0.05). In chondrocytes from OA patients, Beclin 1 overexpression significantly increased cell viability (P<0.05). Beclin 1 overexpression additionally decreased the degree of apoptosis, as demonstrated by Hoechst staining and flow cytometric analysis. B-cell lymphoma-2 (Bcl-2) was upregulated, and Bcl-2 associated X was downregulated, following Beclin 1 overexpression (P<0.05). The PI3K/Akt/mTOR signaling pathway was mitigated following Beclin 1 overexpression (P<0.05). In addition, MMP1, MMP3 and MMP13 were downregulated after Beclin 1 overexpression (P<0.05). Taken together, low expression levels of Beclin 1 may contribute towards the degeneration of chondrocytes. Beclin 1 overexpression increased cell viability, inhibited apoptosis and MMPs, likely via the PI3K/Akt/mTOR signaling pathway.

摘要

在本研究中，研究了自噬相关蛋白 Beclin 1 在骨关节炎（OA）软骨组织中的表达及其在 OA 患者软骨细胞增殖、凋亡和基质金属蛋白酶（MMPs）表达中的作用。采用免疫组织化学、半定量聚合酶链反应和 Western blot 检测 OA 患者和年龄、性别匹配的对照组软骨组织中 Beclin 1 的表达。将软骨细胞分为对照组和 Beclin 1 过表达组。转染 48、72 和 96 h 后，检测细胞活力、凋亡、磷酸肌醇 3-激酶（PI3K）/蛋白激酶 B（Akt）/哺乳动物雷帕霉素靶蛋白（mTOR）信号通路和 MMPs。与性别和年龄匹配的对照组相比，OA 患者软骨组织中 Beclin 1 的 mRNA 和蛋白表达水平明显降低（P<0.05）。在 OA 患者的软骨细胞中，Beclin 1 过表达显著增加了细胞活力（P<0.05）。Beclin 1 过表达还降低了 Hoechst 染色和流式细胞术分析显示的凋亡程度。Beclin 1 过表达后，B 细胞淋巴瘤-2（Bcl-2）上调，Bcl-2 相关 X 下调（P<0.05）。Beclin 1 过表达后，PI3K/Akt/mTOR 信号通路被抑制（P<0.05）。此外，Beclin 1 过表达后 MMP1、MMP3 和 MMP13 下调（P<0.05）。总之，Beclin 1 低表达可能导致软骨细胞退变。Beclin 1 过表达通过 PI3K/Akt/mTOR 信号通路增加细胞活力，抑制凋亡和 MMPs。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8e46/5646975/d279a11e9a4f/MMR-16-04-3958-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8e46/5646975/d218aff6080d/MMR-16-04-3958-g00.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8e46/5646975/585a0272522a/MMR-16-04-3958-g02.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8e46/5646975/d279a11e9a4f/MMR-16-04-3958-g04.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8e46/5646975/d218aff6080d/MMR-16-04-3958-g00.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8e46/5646975/da04282982bb/MMR-16-04-3958-g01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8e46/5646975/585a0272522a/MMR-16-04-3958-g02.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8e46/5646975/2cacd6bf67f9/MMR-16-04-3958-g03.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8e46/5646975/d279a11e9a4f/MMR-16-04-3958-g04.jpg

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