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7-酮胆固醇诱导的微小RNA-107-5p通过靶向MKP1增加破骨细胞的数量和活性。

7-Ketocholesterol-Induced Micro-RNA-107-5p Increases Number and Activity of Osteoclasts by Targeting MKP1.

作者信息

Li Guoen, Sul Ok-Joo, Yu Rina, Choi Hye-Seon

机构信息

Department of Biological Sciences (BK21 Program), University of Ulsan, Ulsan 44610, Korea.

Department of Food and Nutrition, University of Ulsan, Ulsan 44610, Korea.

出版信息

Int J Mol Sci. 2022 Mar 28;23(7):3697. doi: 10.3390/ijms23073697.

Abstract

Osteoclasts (OCs), which are responsible for bone resorption, play a critical role in cholesterol-induced bone loss and recent studies have suggested that various micro-RNAs (miRs) contribute to modulating OCs. We hypothesized that 7-ketocholesterol (7-KC), a metabolite responsible for cholesterol-induced bone loss, induces miR-107-5p, which affects OCs. Overexpression and knock-down of miR-107-5p were performed using miR-107-5p mimic and anti-miR-107-5p, respectively. The effects of miR-107-5p on OCs were analyzed by tartrate-resistant alkaline phosphatase staining, qPCR, and Western blot. MiR-107-5p was upregulated after 7-KC exposure in receptor activator of nuclear factor kappa-Β ligand-stimulated OCs. Furthermore, miR-107-5p upregulation was also observed in tibiae from an atherogenic diet-fed mice compared with mice fed with a normal diet. MiR-107-5p overexpression enhanced the area and number of OCs, whereas inhibiting the endogenous expression of miR-107-5p generated by 7-KC had the opposite effect. Among the possible candidates, mitogen-activated protein kinase phosphatase-1, a stress-responsive dual-specificity phosphatase that inactivates mitogen-activated protein kinase (MKP1), has been proven to be a target gene of miR-107-5p, as demonstrated by the direct interaction between miR-107-5p and the 3'-untranslated region of MKP1. Collectively, our findings demonstrate that 7-KC-induced miR-107-5p promotes differentiation and function of OCs by downregulating MKP1.

摘要

破骨细胞(OCs)负责骨吸收,在胆固醇诱导的骨质流失中起关键作用,最近的研究表明,各种微小RNA(miRs)有助于调节破骨细胞。我们假设7-酮胆固醇(7-KC)是一种导致胆固醇诱导骨质流失的代谢物,可诱导miR-107-5p,进而影响破骨细胞。分别使用miR-107-5p模拟物和抗miR-107-5p对miR-107-5p进行过表达和敲低。通过抗酒石酸酸性磷酸酶染色、定量聚合酶链反应(qPCR)和蛋白质免疫印迹法分析miR-107-5p对破骨细胞的影响。在核因子κB受体激活剂配体刺激的破骨细胞中,7-KC暴露后miR-107-5p上调。此外,与正常饮食喂养的小鼠相比,在动脉粥样硬化饮食喂养的小鼠的胫骨中也观察到miR-107-5p上调。miR-107-5p过表达增加了破骨细胞的面积和数量,而抑制7-KC产生的miR-107-5p的内源性表达则产生相反的效果。在可能的候选基因中,丝裂原活化蛋白激酶磷酸酶-1(一种应激反应双特异性磷酸酶,可使丝裂原活化蛋白激酶失活)已被证明是miR-107-5p的靶基因,miR-107-5p与丝裂原活化蛋白激酶磷酸酶-1的3'非翻译区之间的直接相互作用证明了这一点。总的来说,我们的研究结果表明,7-KC诱导的miR-107-5p通过下调丝裂原活化蛋白激酶磷酸酶-1促进破骨细胞的分化和功能。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/117d/8998300/67b3374e2c86/ijms-23-03697-g001.jpg

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