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Exp Clin Endocrinol Diabetes 2019; 127(06): 387-395
DOI: 10.1055/a-0630-0173
Article
© Georg Thieme Verlag KG Stuttgart · New York

MicroRNA-204-3p Attenuates High Glucose-Induced MPC5 Podocytes Apoptosis by Targeting Braykinin B2 Receptor

Xu Han
1   Department of Traditional Chinese medicine, the First Affiliated Hospital of China Medical University, Shenyang, China
,
Qiaobei Li
2   Department of Ultrasonic Diagnosis, the First Affiliated Hospital of China Medical University, Shenyang, China
,
Chunyan Wang
2   Department of Ultrasonic Diagnosis, the First Affiliated Hospital of China Medical University, Shenyang, China
,
Yinyan Li
2   Department of Ultrasonic Diagnosis, the First Affiliated Hospital of China Medical University, Shenyang, China
› Author Affiliations
Further Information

Publication History

received 22 March 2018
revised 17 April 2018

accepted 08 May 2018

Publication Date:
25 June 2018 (online)

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Abstract

Background Previous study has been reported that braykinin B2 receptor (Bdkrb2) involves in high glucose-induced renal and podocytes injuries. However, there have been some studies with contradictory results that Bdkrb2 has a protective effect on hyperglycemia-induced injuries in vivo and in vitro. The purpose of the present study was carried out to further investigate the post-transcriptional regulatory mechanism of microRNA (miR) in high glucose-treated podocytes by targeting Bdkrb2 signaling in vitro.

Methods The CCK-8 and flow cytometry were performed to measure the cell viability and apoptosis. Gene and protein expression were assayed by RT-qPCR and western blotting, respectively.

Results High glucose treatment decreased cell viability and induced membrane and DNA damage, as well as apoptosis in podocytes. High glucose treatment also increased the expression of Bdkrb2, which was blocked by miR-204-3p mimics transfection in podocytes. Bioinformatics and luciferase reporter activity showed that miR-204-3p was directly targeted to the 3′-untranslated region (3′-UTR) of Bdkrb2. High glucose-induced apoptosis and dysfunction in podocytes were reserved by miR-204-3p mimics transfection, while the effects of miR-204-3p mimics in high glucose-treated podocytes were neutralized by overexpressed Bdkrb2.

Conclusions These findings suggested that miR-204-3p may play a protective role in high glucose-induced apoptosis and dysfunction in podocytes through down-regulation of Bdkrb2.

Key words

podocyte injury - high glucose - microRNA-204-3p - braykinin B2 receptor - posttranscriptional mechanism
 

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