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Long noncoding RNA XIST modulates microRNA-135/CREB1 axis to influence osteogenic differentiation of osteoblast-like cells in mice with tibial fracture healing.

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机构： [1]Department of Orthopaedics, Medical Center of Hip, Luoyang Orthopedic-Traumatological Hospital (Orthopedics Hospital of Henan Province), No.82, Qiming South Road, Fuhe District, Luoyang 471002, Henan, People’s Republic of China [2]Postdoctoral Mobile Station, Guangzhou University of Traditional Chinese Medicine, Guangzhou 510405, Guangdong, People’s Republic of China [3]Luoyang Graduate Training Department, Henan University of Traditional Chinese Medicine, Zhengzhou 450046, Henan, People’s Republic of China [4]Department of Orthopaedics, Institute of Orthopaedics of Guangzhou University of Chinese Medicine (The Third Afliated Hospital of Guangzhou University of Traditional Chinese Medicine), Guangzhou 510240, Guangdong, People’s Republic of China [5]First Clinical Medical College, Guangzhou University of Traditional Chinese Medicine, Guangzhou 510405, Guangdong, People’s Republic of China [6]Department of Orthopaedics Laboratory, Guangzhou University of Traditional Chinese Medicine, Guangzhou 510405, Guangdong, People’s Republic of China

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关键词： Fracture healing Long noncoding RNA XIST microRNA-135 CREB1 TNF-α/RANKL pathway Osteoblast-like cells

摘要：

Fracture healing is a complex event with the involvement of many cell systems, cytokines, as well as mRNAs. Herein, we report the interactions among long noncoding RNA X-inactive specific transcript (XIST)/microRNA-135 (miR-135)/cAMP response element-binding protein 1 (CREB1) axis during fracture healing. We observed increased expression of XIST in patients with long-term unhealed fracture by microarray analysis. Subsequently, a mouse model with tibial fracture and a cell model using osteoblast-like MC3T3-E1 cells were generated. The XIST overexpression during fracture healing decreased proliferation and differentiation of MC3T3-E1 cells, while silencing of XIST facilitated MC3T3-E1 cell growth. Furthermore, miR-135 targeted CREB1 and negatively regulated its expression. XIST acted as a sponge for miR-135, thereby upregulating CREB1 and promoting the activity of the TNF-α/RANKL pathway. Transfection of miR-135 inhibitor or CREB1 overexpression blocked the stimulating effects of XIST knockdown on MC3T3-E1 cell growth. Besides, specific inhibitors of the TNF-α/RANKL pathway reversed the repressive role of XIST in cell osteogenic differentiation. All in all, these findings suggest that XIST knockdown induces the differentiation of osteoblast-like cells via regulation of the miR-135/CREB1/TNF-α/RANKL axis. XIST, as a consequence, represents an attractive therapeutic strategy to accelerate fracture healing.© 2021. Japan Human Cell Society.

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出版当年[2021]版：

大类 | 3 区生物学

小类 | 4 区细胞生物学

最新[2025]版：

大类 | 3 区生物学

小类 | 4 区细胞生物学

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第一作者机构： [1]Department of Orthopaedics, Medical Center of Hip, Luoyang Orthopedic-Traumatological Hospital (Orthopedics Hospital of Henan Province), No.82, Qiming South Road, Fuhe District, Luoyang 471002, Henan, People’s Republic of China [2]Postdoctoral Mobile Station, Guangzhou University of Traditional Chinese Medicine, Guangzhou 510405, Guangdong, People’s Republic of China

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Long noncoding RNA XIST modulates microRNA-135/CREB1 axis to influence osteogenic differentiation of osteoblast-like cells in mice with tibial fracture healing.

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