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

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 diabe...

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Autores principales: Khajehlandi, Mojdeh, Bolboli, Lotfali, Siahkuhian, Marefat, Rami, Mohammad, Tabandeh, Mohammadreza, Khoramipour, Kayvan, Suzuki, Katsuhiko
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8066303/
https://www.ncbi.nlm.nih.gov/pubmed/33806202
http://dx.doi.org/10.3390/biom11040498
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author Khajehlandi, Mojdeh
Bolboli, Lotfali
Siahkuhian, Marefat
Rami, Mohammad
Tabandeh, Mohammadreza
Khoramipour, Kayvan
Suzuki, Katsuhiko
author_facet Khajehlandi, Mojdeh
Bolboli, Lotfali
Siahkuhian, Marefat
Rami, Mohammad
Tabandeh, Mohammadreza
Khoramipour, Kayvan
Suzuki, Katsuhiko
author_sort Khajehlandi, Mojdeh
collection PubMed
description 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.
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spelling pubmed-80663032021-04-25 Endurance Training Regulates Expression of Some Angiogenesis-Related Genes in Cardiac Tissue of Experimentally Induced Diabetic Rats Khajehlandi, Mojdeh Bolboli, Lotfali Siahkuhian, Marefat Rami, Mohammad Tabandeh, Mohammadreza Khoramipour, Kayvan Suzuki, Katsuhiko Biomolecules Article 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. MDPI 2021-03-25 /pmc/articles/PMC8066303/ /pubmed/33806202 http://dx.doi.org/10.3390/biom11040498 Text en © 2021 by the authors. https://creativecommons.org/licenses/by/4.0/Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/ (https://creativecommons.org/licenses/by/4.0/) ).
spellingShingle Article
Khajehlandi, Mojdeh
Bolboli, Lotfali
Siahkuhian, Marefat
Rami, Mohammad
Tabandeh, Mohammadreza
Khoramipour, Kayvan
Suzuki, Katsuhiko
Endurance Training Regulates Expression of Some Angiogenesis-Related Genes in Cardiac Tissue of Experimentally Induced Diabetic Rats
title Endurance Training Regulates Expression of Some Angiogenesis-Related Genes in Cardiac Tissue of Experimentally Induced Diabetic Rats
title_full Endurance Training Regulates Expression of Some Angiogenesis-Related Genes in Cardiac Tissue of Experimentally Induced Diabetic Rats
title_fullStr Endurance Training Regulates Expression of Some Angiogenesis-Related Genes in Cardiac Tissue of Experimentally Induced Diabetic Rats
title_full_unstemmed Endurance Training Regulates Expression of Some Angiogenesis-Related Genes in Cardiac Tissue of Experimentally Induced Diabetic Rats
title_short Endurance Training Regulates Expression of Some Angiogenesis-Related Genes in Cardiac Tissue of Experimentally Induced Diabetic Rats
title_sort endurance training regulates expression of some angiogenesis-related genes in cardiac tissue of experimentally induced diabetic rats
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8066303/
https://www.ncbi.nlm.nih.gov/pubmed/33806202
http://dx.doi.org/10.3390/biom11040498
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