BACKGROUND: The mechanisms responsible for the cardiac dysfunction associated with dietary protein restriction (PR) are poorly understood. Thus, this study was designed to evaluate the effects of PR on calcium kinetics, basal and β-adrenergic contractility in murine ventricular cardiomyocytes. METHODS: After breastfeeding male Fisher rats were distributed into a control group (CG, n = 20) and a protein-restricted group (PRG, n = 20), receiving isocaloric diets for 35 days containing 15% and 6% protein, respectively. Biometric and hemodynamic variables were measured. After euthanasia left ventricles (LV) were collected for histopathological evaluation, SERCA2a expression, cardiomyocytes contractility and Ca(2+)sparks analysis. RESULTS: PRG animals showed reduced general growth, increased heart rate and arterial pressure. These animals presented extracellular matrix expansion and disorganization, cardiomyocytes hypotrophy, reduced amplitudes of shortening and maximum velocity of contraction and relaxation at baseline and after β-adrenergic stimulation. Reduced SERCA2a expression as well as higher frequency and lower amplitude of Ca(2+)sparks were observed in PRG cardiomyocytes. CONCLUSION: The observations reveal that protein restriction induces marked myocardial morphofunctional damage. The pathological changes of cardiomyocyte mechanics suggest the potential involvement of the β-adrenergic system, which is possibly associated with changes in SERCA2a expression and disturbances in Ca(2+) intracellular kinetics.
BACKGROUND: The mechanisms responsible for the cardiac dysfunction associated with dietary protein restriction (PR) are poorly understood. Thus, this study was designed to evaluate the effects of PR on calcium kinetics, basal and β-adrenergic contractility in murine ventricular cardiomyocytes. METHODS: After breastfeeding male Fisher rats were distributed into a control group (CG, n = 20) and a protein-restricted group (PRG, n = 20), receiving isocaloric diets for 35 days containing 15% and 6% protein, respectively. Biometric and hemodynamic variables were measured. After euthanasia left ventricles (LV) were collected for histopathological evaluation, SERCA2a expression, cardiomyocytes contractility and Ca(2+)sparks analysis. RESULTS: PRG animals showed reduced general growth, increased heart rate and arterial pressure. These animals presented extracellular matrix expansion and disorganization, cardiomyocytes hypotrophy, reduced amplitudes of shortening and maximum velocity of contraction and relaxation at baseline and after β-adrenergic stimulation. Reduced SERCA2a expression as well as higher frequency and lower amplitude of Ca(2+)sparks were observed in PRG cardiomyocytes. CONCLUSION: The observations reveal that protein restriction induces marked myocardial morphofunctional damage. The pathological changes of cardiomyocyte mechanics suggest the potential involvement of the β-adrenergic system, which is possibly associated with changes in SERCA2a expression and disturbances in Ca(2+) intracellular kinetics.
Authors: Anna Rebeka Oliveira Ferreira; Maiara Vanusa Guedes Ribeiro; Maria Natalia Chimirri Peres; Silvano Piovan; Géssica Dutra Gonçalves; Lucas Paulo Jacinto Saavedra; Juliana Nunes de Lima Martins; Marcos Divino Ferreira Junior; Keilah Valeria Naves Cavalcante; Gabriel Kian Guimarães Lopes; Mariane Carneiro; Douglas Lopes Almeida; Rodrigo Mello Gomes; Jurandir Fernando Comar; James Andrew Armitage; Paulo Cezar de Freitas Mathias; Kesia Palma-Rigo Journal: Front Physiol Date: 2022-04-28 Impact factor: 4.755
Authors: Sérgio Scalzo; Marcelo Q L Afonso; Néli J da Fonseca; Itamar C G Jesus; Ana Paula Alves; Carolina A T F Mendonça; Vanessa P Teixeira; Diogo Biagi; Estela Cruvinel; Anderson K Santos; Kiany Miranda; Flavio A M Marques; Oscar N Mesquita; Christopher Kushmerick; Maria José Campagnole-Santos; Ubirajara Agero; Silvia Guatimosim Journal: Cell Rep Methods Date: 2021-07-07