International immunopharmacology · 2022
LncRNA KCNQ1OT1 attenuates myocardial injury induced by hip fracture via regulating of miR-224-3p/GATA4 axis.
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Duan Xuzhou, Miao Zhijing, Chen Jia
Аннотация
OBJECTIVE: This article aims to discuss the role of l KCNQ1 opposite strand/antisense transcript 1 (KCNQ1OT1) in myocardial injury caused by a hip fracture and further investigate its potential molecular mechanisms.
METHODS: X-Ray and H&E staining are used to observe hip fracture and pathological changes of myocardial tissue. ELISA and kits are used to detect inflammatory cytokines, lactate dehydrogenase (LDH), and creatine kinase (CK) in serum. The proliferation and apoptosis of H9c2 are determined by CCK-8 and flow cytometry. RT-qPCR and Western blot are applied to quantitatively assess the expression of related genes. Bioinformatics analysis is performed to search the downstream target of KCNQ1OT1 and miR-224-3p. Furthermore, the interaction is verified by a luciferase reporter assay.
RESULTS: A hip fracture model was successfully established. The high expression of inflammatory cytokines and cardiac injury markers indicated that hip fracture successfully induced myocardial injury. In TNF-ɑ treated cardiomyocyte model, high expression of KCNQ1OT1 promoted H9c2 cell proliferation and inhibited apoptosis. Furthermore, in the myocardial injury model rats induced by hip fracture, a high expression of KCNQ1OT1 reduced pathological damage in the myocardial tissue. Further research illustrated that miR-224-3p was the direct target of KCNQ1OT1, and GATA4 was the direct target of miR-224-3p. Importantly, functional research findings indicated that KCNQ1OT1 regulated myocardial injury caused by hip fracture via targeting the miR-224-3p/GATA4 axis.
CONCLUSION: Our study demonstrates that the KCNQ1OT1 suppresses myocardial injury via mediating miR-224-3p/GATA4, which provides a latent target for myocardial injury treatment.
METHODS: X-Ray and H&E staining are used to observe hip fracture and pathological changes of myocardial tissue. ELISA and kits are used to detect inflammatory cytokines, lactate dehydrogenase (LDH), and creatine kinase (CK) in serum. The proliferation and apoptosis of H9c2 are determined by CCK-8 and flow cytometry. RT-qPCR and Western blot are applied to quantitatively assess the expression of related genes. Bioinformatics analysis is performed to search the downstream target of KCNQ1OT1 and miR-224-3p. Furthermore, the interaction is verified by a luciferase reporter assay.
RESULTS: A hip fracture model was successfully established. The high expression of inflammatory cytokines and cardiac injury markers indicated that hip fracture successfully induced myocardial injury. In TNF-ɑ treated cardiomyocyte model, high expression of KCNQ1OT1 promoted H9c2 cell proliferation and inhibited apoptosis. Furthermore, in the myocardial injury model rats induced by hip fracture, a high expression of KCNQ1OT1 reduced pathological damage in the myocardial tissue. Further research illustrated that miR-224-3p was the direct target of KCNQ1OT1, and GATA4 was the direct target of miR-224-3p. Importantly, functional research findings indicated that KCNQ1OT1 regulated myocardial injury caused by hip fracture via targeting the miR-224-3p/GATA4 axis.
CONCLUSION: Our study demonstrates that the KCNQ1OT1 suppresses myocardial injury via mediating miR-224-3p/GATA4, which provides a latent target for myocardial injury treatment.