Lu Liangjie, Wang Lijun, Wu Jiqiong, Yang Minjie, Chen Binhui, Wang Huihan, Gan Kaifeng
Department of Orthopaedics, Ningbo Medical Center, Lihuili Hospital, Ningbo, 315000, China.
Department of Pediatrics, The First Hospital of Jilin University, Changchun, 130021, China.
Epigenomics. 2022 Jun;14(12):777-792. doi: 10.2217/epi-2021-0391. Epub 2022 Jun 29.
This study was designed to elucidate the role of and functions in postmenopausal osteoporosis. Mice were ovariectomized to establish an osteoporosis model and MC3T3-E1-14 osteoblasts were induced to differentiate. Gain- or loss-of-function approaches were used to manipulate the expression of , and , followed by an evaluation of their role in postmenopausal osteoporosis both and . induced methylation of the promoter region, consequently stimulating osteoblast differentiation. elevated , which decreased and inhibited osteoblast differentiation. Inhibition of reduced while increasing expression, thus alleviating postmenopausal osteoporosis in mice. promotes osteoblast differentiation and prevents postmenopausal osteoporosis by regulating the // axis.
本研究旨在阐明[具体物质1]和[具体物质2]功能在绝经后骨质疏松症中的作用。将小鼠去卵巢以建立骨质疏松症模型，并诱导MC3T3-E1-14成骨细胞分化。采用功能获得或功能丧失方法来调控[具体物质1]、[具体物质2]和[具体物质3]的表达，随后评估它们在体内和体外绝经后骨质疏松症中的作用。[具体物质1]诱导[具体基因]启动子区域的甲基化，从而刺激成骨细胞分化。[具体物质2]升高，这降低了[具体物质3]并抑制成骨细胞分化。抑制[具体物质3]可降低[具体物质2]，同时增加[具体物质1]的表达，从而减轻小鼠绝经后骨质疏松症。[具体物质1]通过调节//轴促进成骨细胞分化并预防绝经后骨质疏松症。
