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解偶联蛋白4对软骨细胞增殖和凋亡的影响：其在骨关节炎中的可能作用及调控机制

Effects of UCP4 on the Proliferation and Apoptosis of Chondrocytes: Its Possible Involvement and Regulation in Osteoarthritis.

作者信息

Huang Zhongming, Li Junhua, Du Shaohua, Chen Guangnan, Qi Yiying, Huang Ligang, Xiao Luwei, Tong Peijian

机构信息

Department of Orthopaedic Surgery, Xiaoshan Chinese Medical Hospital, Hangzhou, China.

Department of Orthopaedic Surgery, Affiliated Jiangnan Hospital of Zhejiang Chinese Medical University, Hangzhou, China.

出版信息

PLoS One. 2016 Mar 2;11(3):e0150684. doi: 10.1371/journal.pone.0150684. eCollection 2016.

DOI:10.1371/journal.pone.0150684
PMID:26934480
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC4775028/
Abstract

Reactive oxygen species (ROS)-induced chondrocytes apoptosis plays a key role in osteoarthritis (OA) pathogenesis. Uncoupling protein 4 (UCP4) can protect cells against oxidative stress via reducing ROS production and cell apoptosis. Here, silencing of UCP4 in primary chondrocytes significantly inhibited cell survival, but induced ROS production and cell apoptosis. UCP4 mRNA of cartilage tissues was decreased in osteoarthritis patients, which was negatively correlated with synovial fluid (SF) leptin concentration. Moreover, leptin treatment (5, 10 and 20 ng/ml) of primary cultured chondrocytes significantly decreased mRNA and protein levels of UCP4, but increased ROS production and cell apoptosis in a dose-dependent manner. The effects of leptin treatment (20 ng/ml) on chondrocytes was partially reversed by ectopic expression of UCP4. More importantly, intraarticularly injection of UCP4 adenovirus remarkably alleviate OA progression and cell apoptosis in a rat OA model induced by anterior cruciate ligament transection (ACLT). In conclusion, UCP4, whose expression was suppressed by leptin, may be involved in the ROS production and apoptosis of chondrocytes, thus contributing to the OA pathogenesis.

摘要

活性氧（ROS）诱导的软骨细胞凋亡在骨关节炎（OA）发病机制中起关键作用。解偶联蛋白4（UCP4）可通过减少ROS生成和细胞凋亡来保护细胞免受氧化应激。在此，原代软骨细胞中UCP4的沉默显著抑制细胞存活，但诱导ROS生成和细胞凋亡。骨关节炎患者软骨组织的UCP4 mRNA水平降低，且与滑液（SF）瘦素浓度呈负相关。此外，对原代培养的软骨细胞进行瘦素处理（5、10和20 ng/ml）可显著降低UCP4的mRNA和蛋白水平，但以剂量依赖方式增加ROS生成和细胞凋亡。UCP4的异位表达部分逆转了瘦素处理（20 ng/ml）对软骨细胞的影响。更重要的是，在由前交叉韧带横断（ACLT）诱导的大鼠OA模型中，关节内注射UCP4腺病毒可显著减轻OA进展和细胞凋亡。总之，UCP4的表达受瘦素抑制，可能参与软骨细胞的ROS生成和凋亡，从而促成OA发病机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c970/4775028/e62bb612a688/pone.0150684.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c970/4775028/ec4998ca0042/pone.0150684.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c970/4775028/2e0c9b59f7ac/pone.0150684.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c970/4775028/f2ec82f9c04e/pone.0150684.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c970/4775028/f8db36b8569a/pone.0150684.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c970/4775028/e62bb612a688/pone.0150684.g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c970/4775028/ec4998ca0042/pone.0150684.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c970/4775028/2e0c9b59f7ac/pone.0150684.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c970/4775028/f2ec82f9c04e/pone.0150684.g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c970/4775028/f8db36b8569a/pone.0150684.g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/c970/4775028/e62bb612a688/pone.0150684.g005.jpg

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引用本文的文献

[1]
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[2]
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[3]
Mitochondrial Uncoupling Proteins (UCPs) as Key Modulators of ROS Homeostasis: A Crosstalk between Diabesity and Male Infertility?

Antioxidants (Basel). 2021-10-30

[4]
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Exp Ther Med. 2021-2

[5]
BNIP3 decreases the LPS-induced inflammation and apoptosis of chondrocytes by promoting the development of autophagy.

J Orthop Surg Res. 2020-7-28

[6]
Mitochondrial Uncoupling Proteins: Subtle Regulators of Cellular Redox Signaling.

Antioxid Redox Signal. 2018-3-14

[7]
Influence of protein kinase RIPK4 expression on the apoptosis and proliferation of chondrocytes in osteoarthritis.

Mol Med Rep. 2017-12-7

[8]
Electroacupuncture serum inhibits TNF‑α‑mediated chondrocyte inflammation via the Ras‑Raf‑MEK1/2‑ERK1/2 signaling pathway.

Mol Med Rep. 2017-8-28

[9]
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本文引用的文献

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Mitochondrial UCP4 mediates an adaptive shift in energy metabolism and increases the resistance of neurons to metabolic and oxidative stress.

Neuromolecular Med. 2006

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