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STAMP2通过抑制2型糖尿病大鼠中NMRAL1介导的NF-κB减轻糖尿病心肌病中的心脏功能障碍和胰岛素抵抗。

STAMP2 Attenuates Cardiac Dysfunction and Insulin Resistance in Diabetic Cardiomyopathy via NMRAL1-Mediated NF-κB Inhibition in Type 2 Diabetic Rats.

作者信息

Gao Zhan, Ti Yun, Lu Bin, Song Fang-Qiang, Zhang Lei, Hu Bo-Ang, Xie Jia-Ying, Zhang Wei, Han Lu, Zhong Ming

机构信息

The Key Laboratory of Cardiovascular Remodeling and Function Research, Chinese Ministry of Education, Chinese National Health Commission and Chinese Academy of Medical Sciences, The State and Shandong Province Joint Key Laboratory of Translational Cardiovascular Medicine, Department of Cardiology, Qilu Hospital, Qilu College of Medicine, Shandong University, Jinan, People's Republic of China.

Department of Cardiology, The First Affiliated Hospital of Wenzhou Medical University, Wenzhou, People's Republic of China.

出版信息

Diabetes Metab Syndr Obes. 2022 Oct 20;15:3219-3229. doi: 10.2147/DMSO.S374784. eCollection 2022.

DOI:10.2147/DMSO.S374784
PMID:36276296
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9581721/
Abstract

BACKGROUND

Previous studies have reported that six transmembrane protein of prostate 2 (STAMP2) attenuates metabolic inflammation and insulin resistance in diabetes mellitus. However, the role of STAMP2 in the diabetic heart is still unclear.

METHODS

A diabetic rat cardiomyopathy model was established via intraperitoneal STZ injection. STAMP2 was overexpressed in the treatment group using adeno-associated virus. Rat heart diastolic function was measured using echocardiography and a left ventricular catheter, and cardiac interstitial fibrosis was detected by immunohistochemistry and histological staining. Insulin sensitivity and NF-κB expression were shown by Western blotting. NMRAL1 distribution was illustrated by immunofluorescence.

RESULTS

STAMP2 expression in the diabetic rat heart was reduced, and exogenous overexpression of STAMP2 improved glucose tolerance and insulin sensitivity and alleviated diastolic dysfunction and myocardial fibrosis. Furthermore, we found that NF-κB signaling is activated in the diabetic heart and that exogenous overexpression of STAMP2 promotes NMRAL1 translocation from the cytoplasm to the nucleus and inhibits p65 phosphorylation.

CONCLUSION

STAMP2 attenuates cardiac dysfunction and insulin resistance in diabetic cardiomyopathy, likely by promoting NMRAL1 retranslocation and NF-κB signaling inhibition.

摘要

背景

既往研究报道，前列腺六跨膜蛋白2（STAMP2）可减轻糖尿病中的代谢性炎症和胰岛素抵抗。然而，STAMP2在糖尿病心脏中的作用仍不清楚。

方法

通过腹腔注射链脲佐菌素建立糖尿病大鼠心肌病模型。使用腺相关病毒在治疗组中过表达STAMP2。用超声心动图和左心室导管测量大鼠心脏舒张功能，通过免疫组织化学和组织学染色检测心脏间质纤维化。通过蛋白质免疫印迹显示胰岛素敏感性和核因子κB（NF-κB）表达。通过免疫荧光说明NMRAL1分布。

结果

糖尿病大鼠心脏中STAMP2表达降低，外源性过表达STAMP2可改善葡萄糖耐量和胰岛素敏感性，并减轻舒张功能障碍和心肌纤维化。此外，我们发现糖尿病心脏中NF-κB信号通路被激活，外源性过表达STAMP2可促进NMRAL1从细胞质向细胞核易位并抑制p65磷酸化。

结论

STAMP2可能通过促进NMRAL1重新易位和抑制NF-κB信号通路减轻糖尿病心肌病中的心脏功能障碍和胰岛素抵抗。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dabe/9581721/a2b512ea92ff/DMSO-15-3219-g0007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dabe/9581721/371114da6358/DMSO-15-3219-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dabe/9581721/d208d90de59a/DMSO-15-3219-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dabe/9581721/74e823872426/DMSO-15-3219-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dabe/9581721/5b9ffdb99863/DMSO-15-3219-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dabe/9581721/834163a34b04/DMSO-15-3219-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dabe/9581721/52024bff38da/DMSO-15-3219-g0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dabe/9581721/a2b512ea92ff/DMSO-15-3219-g0007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dabe/9581721/371114da6358/DMSO-15-3219-g0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dabe/9581721/d208d90de59a/DMSO-15-3219-g0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dabe/9581721/74e823872426/DMSO-15-3219-g0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dabe/9581721/5b9ffdb99863/DMSO-15-3219-g0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dabe/9581721/834163a34b04/DMSO-15-3219-g0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dabe/9581721/52024bff38da/DMSO-15-3219-g0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/dabe/9581721/a2b512ea92ff/DMSO-15-3219-g0007.jpg

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