Endurance Training Regulates Expression of Some Angiogenesis-Related Genes in Cardiac Tissue of Experimentally Induced Diabetic Rats.

Mojdeh Khajehlandi,Lotfali Bolboli,Marefat Siahkuhian,Kayvan Khoramipour,Mohammadreza Tabandeh,Katsuhiko Suzuki,Mohammad Rami

doi:10.3390/biom11040498

Abstract

Exercise can ameliorate cardiovascular dysfunctions in the diabetes condition, but its precise molecular mechanisms have not been entirely understood. The aim of the present study was to determine the impact of endurance training on expression of angiogenesis-related genes in cardiac tissue of diabetic rats. Thirty adults male Wistar rats were randomly divided into three groups (N = 10) including diabetic training (DT), sedentary diabetes (SD), and sedentary healthy (SH), in which diabetes was induced by a single dose of streptozotocin (50 mg/kg). Endurance training (ET) with moderate-intensity was performed on a motorized treadmill for six weeks. Training duration and treadmill speed were increased during five weeks, but they were kept constant at the final week, and slope was zero at all stages. Real-time polymerase chain reaction (RT-PCR) analysis was used to measure the expression of myocyte enhancer factor-2C (MEF2C), histone deacetylase-4 (HDAC4) and Calmodulin-dependent protein kinase II (CaMKII) in cardiac tissues of the rats. Our results demonstrated that six weeks of ET increased gene expression of MEF2C significantly (p < 0.05), and caused a significant reduction in HDAC4 and CaMKII gene expression in the DT rats compared to the SD rats (p < 0.05). We concluded that moderate-intensity ET could play a critical role in ameliorating cardiovascular dysfunction in a diabetes condition by regulating the expression of some angiogenesis-related genes in cardiac tissues.

Highlights

Researchers found new players in the angiogenesis process that are regulated by a complex network of transcriptional factors including myocyte enhancer factor-2C (MEF2C), histone deacetylase4 (HDAC4), and Calmodulin-dependent protein kinase II (CaMKII) [10]
This is the first study that examined the effect of moderate-intensity Endurance training (ET) on MEF2C, HDAC4, and CaMKII gene expression and testosterone levels in diabetic hearts
Our results showed that ET controlled serum levels of glucose, increased MEF2C, and decreased HDAC4 and CaMKII gene expression and rose serum testosterone levels in diabetic rats

Summary

Introduction

Researchers found new players in the angiogenesis process that are regulated by a complex network of transcriptional factors including myocyte enhancer factor-2C (MEF2C), histone deacetylase (HDAC4), and Calmodulin-dependent protein kinase II (CaMKII) [10]. HDACs control biological processes by de-acetylation of histone and regulating accessibility of transcription factors to the gene promoter [14]. Among all HDACs, HDAC4 plays an important role in mediating cardiovascular diseases [15]. This transcription factor is phosphorylated and activated by CaMKII, a central culprit in the development of heart failure and cardiac arrhythmia [16], and negatively interacts with MEF2C to control its repressive activity [17]. The activities of HDAC4 and CaMKII (representatives of histone acetylation) are increased in the diabetic condition [18,19]

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