Small Heat Shock Proteins HSP10 and HSP27 in the Left Ventricular Myocardium in Rats with Arterial Hypertension and Insulin-Dependent Diabetes Mellitus

We studied the expression of small heat shock proteins HSP10 and HSP27 in left ventricular cardiomyocytes in animals with arterial hypertension, insulin-dependent diabetes mellitus, and their combination. The experiment was performed on 38-week-old male Wistar-Kyoto and 38-57-week-old SHR (spontaneously hypertensive) rats. Insulin-dependent diabetes mellitus was modeled by single parenteral injection of streptozotocin (65 mg/kg). Expression of HSP10 and HSP27 in left ventricular cardiomyocytes was evaluated by immunohistochemical assay. It was found that the content of HSP10 in the left ventricular cardiomyocytes decreased in comparison with the control in case of isolated diabetes mellitus and, on the contrary, increased in case of arterial hypertension combined with diabetes mellitus. The intensity of HSP27 expression decreased in case of 38-week arterial hypertension and a combination of arterial hypertension with diabetes mellitus. However, in case of 57-week arterial hypertension we observed an increase in the content of HSP27 in cardiomyocytes

Beclin-1-Dependent Autophagy of Left Ventricular Cardiomyocytes in SHR and Wistar-Kyoto Rats with Type 1 Diabetes Mellitus

Autophagy is considered as a mechanism of progression of heart failure, but under certain conditions, it can also act as an adaptation mechanism. Beclin-1 plays the key role in autophagy. We studied the features of Beclin-1 expression in cardiomyocytes of the left ventricle in arterial hypertension, type 1 diabetes mellitus, and their combination. The experiment was performed on male 38-week-old Wistar Kyoto rats and SHR rats aged 38 and 57 weeks. Type 1 diabetes mellitus was modeled by a single parenteral administration of streptozotocin. Expression of Beclin-1 in cardiomyocytes of the left ventricle was evaluated by immunohistochemical analysis. In arterial hypertension, a decrease in the intensity of Beclin-1-dependent autophagy of cardiomyocytes was seen, while in combined pathology, we observed an opposite effect manifested as a significant increase in the expression of protein Beclin-1. © 2021, Springer Science+Business Media, LLC, part of Springer Nature

Expression of Bax and Bcl-2 Proteins in Left-Ventricular Cardiomyocytes in Wistar-Kyoto and SHR Rats with Insulin-Dependent Diabetes Mellitus

Loss of cardiomyocytes due to apoptotic or necrotic death is an important component of the pathogenesis of heart failure. Initiation of apoptosis by the mitochondrial pathway depends on the balance between proapoptotic and antiapoptotic factors, in particular, Bax and Bcl-2. Cardiomyocyte apoptosis in essential hypertension is studied in sufficient details. At the same time, apoptotic processes in the myocardium in diabetes mellitus alone and in combination with essential hypertension remain poorly understood. Here we studied the expression of Bax and Bcl-2 in the left ventricular cardiomyocytes of 38-week-old male Wistar-Kyoto rats and 38- and 57-week-old SHR rats with essential hypertension, diabetes mellitus, and a combination of these pathologies. Insulin-dependent diabetes mellitus was modelled by a single parenteral administration of streptozotocin in a dose 65 mg/kg. Expression of Bax and Bcl-2 was assessed by the immunohistochemical method. In essential hypertension and diabetes mellitus, the apoptotic processes in the ventricular myocardium were enhanced, as is seen from the increase in the content of the proapoptotic factor Bax and a decrease in the expression of the antiapoptotic factor Bcl-2. However, in case of combined pathology, Bax content increased less markedly, while the expression of antiapoptotic Bcl-2 was significantly increased. © 2021, Springer Science+Business Media, LLC, part of Springer Nature

Heat Shock Protein HSP60 in Left Ventricular Cardiomyocytes of Hypertensive Rats with and without Insulin-Dependent Diabetes Mellitus

In cardiomyocytes, high molecular ATP-dependent HSP70 and HSP90 play an important role in protecting the myocardium from abnormal proteins that appear, in particular, due to activation of oxidative stress. Molecular chaperone HSP60 is of particular importance for cardiomyocytes as it is responsible for assembly of mitochondrial matrix proteins. We studied the peculiarities of expression of HSP60 in left ventricular cardiomyocytes in hypertension, insulin-dependent diabetes mellitus, and their combination. The experiment was performed on 38-week-old male Wistar-Kyoto and SHR (spontaneously hypertensive) rats aged 38-57 weeks. Insulin-dependent diabetes mellitus was modeled by a single parenteral administration of 65 mg/kg streptozotocin. Expression of HSP60 in left ventricular cardiomyocytes was evaluated by immunohistochemical methods. It was found that hypertension, diabetes mellitus, and their combination are associated with a significant decrease in the content of HSP60 in left ventricular cardiomyocytes in comparison with the control. This finding can be considered as a pathogenetic mechanism of myocardial damage induced by hypertension and diabetes mellitus. © 2020, Springer Science+Business Media, LLC, part of Springer Nature

BCL2-regulated apoptotic process in myocardial ischemia-reperfusion injury (Review)

The leading cause of death in developed countries is cardiovascular disease, where coronary heart disease is the main cause of death. Myocardial reperfusion is the most significant method to prevent cell death after ischemia. However, restoration of blood flow may paradoxically lead to myocardial ischemia-reperfusion injury (MI/RI) accompanied by metabolic disturbances and cardiomyocyte death. As the myocardium has an extremely limited ability to regenerate, the mechanisms of regulated cell death, including apoptosis, are the most significant for contemporary research due to their reversibility. BCL2 is a key anti-apoptotic protein. There are several signaling pathways and compounds regulating BCL2, including PI3K/AKT and MEK1/ERK1/2, JAK2/STAT3, endothelial nitric oxide synthase, PTEN, cardiac ankyrin repeat protein and microRNA, which can serve as targets for modern methods of cardioprotective therapy inhibiting intrinsic apoptosis and saving viable cardiomyocytes after MI/RI. The present review considers the mechanisms of Bcl2-regulated apoptosis in the development and treatment of MI/RI. © This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0) License