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Changes of miR-34a and GPS2 expression and their effects on JNK pathway protein in acute kidney injury |
CHEN Weiwei1, WANG Dexuan2, SHEN Meng1, ZHUANG Jieqiu2, CAI Hui1 |
1.Department of Nephrology, the Second Affiliated Hospital & Yuying Children’s Hospital of Wenzhou Medical University, Wenzhou 325027, China; 2.Department of Pediatrics Nephrology, the Second Affiliated Hospital & Yuying Children’s Hospital of Wenzhou Medical University, Wenzhou 325027, China |
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Cite this article: |
CHEN Weiwei,WANG Dexuan,SHEN Meng, et al. Changes of miR-34a and GPS2 expression and their effects on JNK pathway protein in acute kidney injury[J]. JOURNAL OF WEZHOU MEDICAL UNIVERSITY, 2020, 50(6): 438-443.
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Abstract Objective: To explore the expression changes of miR-34a and GPS2 and their effects on p-JNK in ischemia-reperfusion and hypoxia/reoxygenation models. Methods: Thirty SD rats were randomly divided into 6 groups (n=5). Serum and kidney tissues were collected from the perfusion control group (0 h, 24 h, 48 h) and the perfusion model group (0 h, 24 h, 48 h). HEK 293T cells were divided into control group (Control, NC inhibitor) and model group (Model, Model+miR-34a inhbitor). RNA and protein were extracted from the cells.The levels of tumor necrosis factor (TNF-α) and transforming growth factor (TGF-β) in serum were measured by ELISA kit. The pathological changes of kidney tissues were compared by hematoxylin-eosin (HE). The mRNA changes of miR-34a and GPS2 were detected by RT-qPCR, and the protein expressions of GPS2 and p-JNK were detected by Western blot. Results: HE results showed that renal tubular injury in the model group had epithelial cell swelling, brush edge disappearance and vacuolation formation, compared with the control group. ELISA results showed that there was no difference in TNF-α and TGF-β levels between the model group and the control group before and after the establishment of the model. TNF-α and TGF-β levels in the model group increased with the perfusion time and significantly higher than the respective control group (P<0.01). Compared with the control group, the damage of renal tubules in the model group had swelling of epithelial cells, disappearance of brush border and formation of vacuoles. The expressions of miR-34a and p-JNK increased in the model group (P<0.05), while GPS2 decreased (P<0.05). Cell PCR and Western blot show that GPS2 increased significantly (P<0.05) and p-JNK decreased significantly (P<0.05) after miR-34a was silenced. Conclusion: miR-34a may indirectly activate JNK pathway through GPS2, and then promotes and aggravates the occurrence of acute kidney injury.
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Received: 15 September 2019
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