Loading…

Expression of transient receptor potential vanilloid genes and proteins in diabetic rat heart

Cardiac complications are leading causes of death in diabetic patients. Imbalance of Ca 2+ homeostasis is a hallmark of cardiac dysfunction in diabetes, while TRPV channels are non-selective for cations and are permeable to Ca 2+ . Our aim was to evaluate the expression levels of TRPV1, TRPV2, TRPV3...

Full description

Saved in:
Bibliographic Details
Published in:Molecular biology reports 2021-02, Vol.48 (2), p.1217-1223
Main Authors: Jia, Xiaoli, Yu, Tao, Xiao, Chao, Sheng, Deqiao, Yang, Mengcheng, Cheng, Quanyi, Wu, Jing, Lian, Ting, Zhao, Yun, Zhang, Shizhong
Format: Article
Language:English
Subjects:
Citations: Items that this one cites
Items that cite this one
Online Access:Get full text
Tags: Add Tag
No Tags, Be the first to tag this record!
Description
Summary:Cardiac complications are leading causes of death in diabetic patients. Imbalance of Ca 2+ homeostasis is a hallmark of cardiac dysfunction in diabetes, while TRPV channels are non-selective for cations and are permeable to Ca 2+ . Our aim was to evaluate the expression levels of TRPV1, TRPV2, TRPV3, TRPV4, TRPV5, and TRPV6 genes and proteins in cardiac tissue at 3 days and 4, 8, and 12 weeks after induction of diabetes. Sprague-Dawley rats were assigned to control and DM groups. DM was induced by intraperitoneal injection of streptozotocin (60 mg/kg). The expression levels of TRPV genes were analyzed by the quantitative reverse transcription polymerase chain reaction, and TRPV proteins were determined by western blotting. Compared to controls, the expression levels of TRPV2, TRPV3, and TRPV6 in diabetic myocardium did not change, while TRPV1 decreased at 4, 8, and 12 weeks, TRPV4 was upregulated at 3 days and 4, 8, and 12 weeks, TRPV5 mRNA increased at 8 and 12 weeks, and TRPV5 protein increased at 4, 8, and 12 weeks. Our findings showed that TRPV1, TRPV4, and TRPV5 are associated with the diabetic heart.
ISSN:0301-4851
1573-4978
DOI:10.1007/s11033-021-06182-7