期刊
MOLECULAR THERAPY-NUCLEIC ACIDS
卷 23, 期 -, 页码 1345-1359出版社
CELL PRESS
DOI: 10.1016/j.omtn.2021.02.008
关键词
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资金
- National Natural Science Foundation of China [81772345]
- National Key Research & Development Program of China [2018YFC2001502, 2018YFB1105705]
- National Health Commission of the People's Republic of China [ZX-01-018, ZX-01-C2016153]
- Health Commission of Hubei Province [WJ2019Z009]
This study revealed that TBI-induced upregulation of miRNA-92a-3p inhibits IBSP expression, accelerates osteoblast differentiation, and promotes fracture healing. IBSP regulates osteoblast differentiation through the PI3K/AKT signaling pathway. Pre-injection of agomiR92a-3p enhances bone formation. Overexpression of miRNA-92a-3p may be a key factor in the improved fracture healing observed in TBI patients.
Patients who sustain concomitant fractures and traumatic brain injury (TBI) are known to have significantly quicker fracture-healing rates than patients with isolated fractures. The mechanisms underlying this phenomenon have yet to be identified. In the present study, we found that the upregulation of microRNA-92a-3p (miRNA-92a-3p) induced by TBI correlated with a decrease in integrin binding sialoprotein (IBSP) expression in callus formation. In vitro, overexpressing miRNA-92a3p inhibited IBSP expression and accelerated osteoblast differentiation, whereas silencing of miRNA-92a-3p inhibited osteoblast activity. A decrease in IBSP facilitated osteoblast differentiation via the Phosphatidylinositol 3-kinase/threonine kinase 1 (PI3K/AKT) signaling pathway. Through luciferase assays, we found evidence that IBSP is a miRNA-92a-3p target gene that negatively regulates osteoblast differentiation. Moreover, the present study confirmed that pre-injection of agomiR92a-3p leads to increased bone formation. Collectively, these results indicate that miRNA-92a-3p overexpression may be a key factor underlying the improved fracture healing observed in TBI patients. Upregulation of miRNA-92a-3p may therefore be a promising therapeutic strategy for promoting fracture healing and preventing nonunion.
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