Dexamethasone Does Not Inhibit Treadmill Training-Induced Angiogenesis in Myocardium: Role of MicroRNA-126 Pathway

Autor(es)

Herrera, Naiara A. ^[1] ; Duchatsch, Francine ^[1] ; Tardelli, Lidieli P. ^[1] ; Dionisio, Thiago J. ^[2] ; Santos, Carlos F. ^[2] ; Amaral, Sandra L. ^{[3, 1]}

Afiliação do(s) autor(es)

^[1] PIPGCF UFSCar UNESP, Joint Grad Program Physiol Sci, Sao Carlos, SP - Brazil

^[2] Univ Sao Paulo, Bauru Sch Dent, Dept Biol Sci, Bauru, SP - Brazil

^[3] Sao Paulo State Univ Unesp, Sch Sci, Dept Phys Educ, Bauru, SP - Brazil

• Tipo de documento: Artigo Científico
• Fonte: Journal of Cardiovascular Pharmacology; v. 76, n. 6, p. 708-714, DEC 2020.
• Citações Web of Science: 1

Resumo

Dexamethasone (DEX) has important anti-inflammatory activities; however, it induces hypertension and skeletal muscle microcirculation rarefaction. Nevertheless, nothing is known about DEX outcomes on cardiac microcirculation. By contrast, exercise training prevents skeletal and cardiac microvessel loss because of microRNA expression and a better balance between their related angiogenic and apoptotic proteins in spontaneously hypertensive rats. The purpose of this study was to investigate whether DEX and/or exercise training could induce microRNA alterations leading to cardiac angiogenesis or microvascular rarefaction. Animals performed 8 weeks of exercise training and were treated with DEX (50 mu g/kg per day, subcutaneously) for 14 days. Cardiovascular parameters were measured, and the left ventricle muscle was collected for analyses. DEX treatment increased arterial pressure and did not cause cardiac microcirculation rarefaction. Treadmill training prevented the DEX-induced increase in arterial pressure. In addition, training, regardless of DEX treatment, increased microRNA-126 expression, phospho-protein kinase B/protein kinase B, and endothelial nitric oxide synthase levels associated with cardiac angiogenesis. In conclusion, this study suggests, for the first time, that treadmill training induces myocardial angiogenesis because of angiogenic pathway improvement associated with an increase in microRNA-126. Furthermore, DEX, per se, did not cause capillary density alterations and did not attenuate cardiac angiogenesis induced by training. (AU)

• Processo FAPESP: 18/06998-7 - Treinamento físico previne rarefação induzida por dexametasona: papel da mitocôndria
• Beneficiário: Naiara Araújo Herrera
• Modalidade de apoio: Bolsas no Exterior - Estágio de Pesquisa - Doutorado
• Processo FAPESP: 17/00509-1 - Papel do treinamento físico no balanço autonômico, rigidez arterial e rarefação em ratos espontaneamente hipertensos tratados com dexametasona: contribuição dos microRNAs
• Beneficiário: Sandra Lia do Amaral Cardoso
• Modalidade de apoio: Auxílio à Pesquisa - Regular
• Processo FAPESP: 16/12532-5 - A INFLUÊNCIA DO TREINAMENTO FÍSICO EM RATOS ESPONTANEAMENTE HIPERTENSOS TRATADOS COM DEXAMETASONA: CONTRIBUIÇÃO DOS MICRORNAs
• Beneficiário: Naiara Araújo Herrera
• Modalidade de apoio: Bolsas no Brasil - Doutorado
• Processo FAPESP: 17/14405-3 - Influência do treinamento físico aeróbio no remodelamento cardíaco de ratos espontaneamente hipertensos tratados com dexametasona
• Beneficiário: Francine Duchatsch Ribeiro de Souza
• Modalidade de apoio: Bolsas no Brasil - Mestrado
• Processo FAPESP: 15/03965-2 - Papel do sistema renina-angiotensina em diferentes modelos inflamatórios orais: uma abordagem interdisciplinar experimental e clínica
• Beneficiário: Carlos Ferreira dos Santos
• Modalidade de apoio: Auxílio à Pesquisa - Temático