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一种新型长链非编码RNA，Lnc-OAD，是骨形态发生蛋白2（BMP-2）诱导成骨细胞分化所必需的。

A Novel Long Noncoding RNA, Lnc-OAD, Is Required for Bone Morphogenetic Protein 2- (BMP-2-) Induced Osteoblast Differentiation.

作者信息

Wang Zonggui, Zhou Yanfang, Dai Zhong, Chen Xiuju, Li Chuyu, Lin Zhanying, Wu Huixing, Li Siqi, Zuo Changqing

机构信息

Department of Biochemistry and Molecular Biology, Guangdong Provincial Key Laboratory of Medical Molecular Diagnostics, Guangdong Medical University, Dongguan, China.

Department of Pathophysiology, Guangdong Medical University, Dongguan, China.

出版信息

Biomed Res Int. 2021 Mar 16;2021:6697749. doi: 10.1155/2021/6697749. eCollection 2021.

DOI:10.1155/2021/6697749
PMID:33816629
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7987440/
Abstract

Long noncoding RNAs (lncRNAs) play very important roles in cell differentiation. Our recent study has demonstrated that a novel lncRNA named lnc-OAD modulated 3T3-L1 adipocyte differentiation. In the present study, we examined the roles of lnc-OAD in bone morphogenetic protein 2- (BMP-2-) induced osteoblast differentiation. Lnc-OAD expression was increased during BMP-2-induced osteoblast differentiation in C3H10T1/2 mesenchymal stem cells and MC3T3-E1 preosteoblast cells. Knockdown of lnc-OAD expression by specific siRNA remarkably decreased early osteoblast differentiation. In addition, stable knockdown of lnc-OAD by lentivirus vector also significantly inhibited late osteoblast differentiation and matrix mineralization in vitro. Conversely, stably overexpressed lnc-OAD with lentiviral vector accelerated osteoblast differentiation. Mechanistically, knockdown of lnc-OAD reduced significantly the phosphorylation of AKT and the expression of Osterix induced by BMP-2, while overexpression of lnc-OAD enhanced the phosphorylation of AKT and the expression of Osterix. Taken together, our study suggests that lnc-OAD plays an important role in modulating BMP-2-induced osteoblast differentiation via, at least in part, regulating the AKT-Osterix signaling axis.

摘要

长链非编码RNA（lncRNAs）在细胞分化中发挥着非常重要的作用。我们最近的研究表明，一种名为lnc-OAD的新型lncRNA可调节3T3-L1脂肪细胞分化。在本研究中，我们检测了lnc-OAD在骨形态发生蛋白2（BMP-2）诱导的成骨细胞分化中的作用。在C3H10T1/2间充质干细胞和MC3T3-E1前成骨细胞中，BMP-2诱导成骨细胞分化过程中lnc-OAD表达增加。用特异性siRNA敲低lnc-OAD表达可显著降低早期成骨细胞分化。此外，用慢病毒载体稳定敲低lnc-OAD也显著抑制了体外晚期成骨细胞分化和基质矿化。相反，用慢病毒载体稳定过表达lnc-OAD可加速成骨细胞分化。机制上，敲低lnc-OAD可显著降低BMP-2诱导的AKT磷酸化和osterix表达，而过表达lnc-OAD则增强AKT磷酸化和osterix表达。综上所述，我们的研究表明lnc-OAD至少部分通过调节AKT-osterix信号轴在调节BMP-2诱导的成骨细胞分化中起重要作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5373/7987440/a5a4398e906a/BMRI2021-6697749.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5373/7987440/6df3ba9e9dad/BMRI2021-6697749.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5373/7987440/9950fe970039/BMRI2021-6697749.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5373/7987440/51143d2c0186/BMRI2021-6697749.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5373/7987440/f729d6ee197c/BMRI2021-6697749.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5373/7987440/4a9b8dc60216/BMRI2021-6697749.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5373/7987440/0b3c86efc2ec/BMRI2021-6697749.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5373/7987440/a5a4398e906a/BMRI2021-6697749.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5373/7987440/6df3ba9e9dad/BMRI2021-6697749.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5373/7987440/9950fe970039/BMRI2021-6697749.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5373/7987440/51143d2c0186/BMRI2021-6697749.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5373/7987440/f729d6ee197c/BMRI2021-6697749.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5373/7987440/4a9b8dc60216/BMRI2021-6697749.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5373/7987440/0b3c86efc2ec/BMRI2021-6697749.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/5373/7987440/a5a4398e906a/BMRI2021-6697749.007.jpg

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