Long non‑coding (lnc)RNA KCNQ1 opposite strand/antisense transcript 1 (Kcnq1ot1) has been shown to regulate multiple biological processes. However, the functional role of Kcnq1ot1 in osteoporosis and the underlying mechanism are still unclear. The present study aimed to investigate the function of lncRNA Kcnq1ot1 in osteogenic differentiation. Alkaline phosphatase (ALP) activity was measured using an ALP assay kit. Western blotting was performed to assess the expression levels of osteogenic differentiation‑associated proteins. Reverse transcription‑quantitative PCR was performed to detect Kcnq1ot1, microRNA (miR)‑98‑5p and T‑box transcription factor 5 (Tbx5) expression levels. The binding of Kcnq1ot1 with miR‑98‑5p and that of miR‑98‑5p with Tbx5 were predicted by starBase and TargetScan databases, respectively, and verified using dual luciferase reporter assays. The mineralization of MC3T3‑E1 cells was observed using an Alizarin red S staining assay. The results revealed that expression of Kcnq1ot1 was increased and that of miR‑98‑5p was decreased during osteogenic differentiation. Additionally, Kcnq1ot1 was shown to target miR‑98‑5p and inhibit its expression. Inhibiting miR‑98‑5p reversed the inhibitory effect of Kcnq1ot1 knockdown on osteogenic differentiation and mineralization of MC3T3‑E1 cells. Furthermore, Kcnq1ot1 regulated Tbx5 expression via miR‑98‑5p. Overexpressing miR‑98‑5p or downregulating Tbx5 expression reversed the promotive effect of Kcnq1ot1 overexpression on osteogenic differentiation and mineralization of MC3T3‑E1 cells. In conclusion, these findings suggested that Kcnq1ot1 may promote bone formation by inhibiting miR‑98‑5p and upregulating Tbx5. Kcnq1ot1, miR‑98‑5p and Tbx5 may therefore serve as promising targets for the treatment of osteoporosis.
Cerebral ischemia/reperfusion (I/R) injury is an obstacle in treating ischemic stroke effectively. miR-98-5p has been reported to have the ability of reducing myocardial I/R injury. To explore the function of miR-98-5p in cerebral I/R, we established mice model of middle cerebral artery occlusion and reperfusion (MCAO/R). The level of miR-98-5p was found to be downregulated in serum of stroke patients and brain tissues of MCAO/R mice. Examination of brain tissues indicated that upregulating miR-98-5p level alleviated the infarction in MCAO/R mice. Moreover, the upregulation of miR-98-5p reduced reactive oxygen species production and enhanced superoxide dismutase activity in brain tissues of MCAO/R mice. These results indicating that miR-98-5p could protect against oxidative stress. Further study showed that miR-98-5p inhibited apoptosis by reducing the levels of death-associated protein kinase 1, B cell lymphoma/leukaemia-2 associated x protein and cleaved caspase-3, as well as increasing the level of B cell lymphoma/leukaemia-2. In addition, miR-98-5p was found to protect against oxidative stress through downregulating the level of BTB domain and CNC homology 1 and upregulating the levels of NAD(P)H: quinone oxidoreductase 1 and heme oxygenase 1. Therefore, miR-98-5p might be a potential target to treat cerebral I/R injury.
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