Hyperglycemia and hyperlipidemia can induce morphophysiological changes in rat cardiac cell line

Abstract

H9c2 cardiac cells were incubated under the control condition and at different hyperglycemic and hyperlipidemic media, and the following parameters were determined and quantified: a) cell death, b) type of cell death, and c) changes in cell length, width and height. Of all the proven media, the one that showed the greatest differences compared to the control was the medium glucose (G) 33 mM + 500 μM palmitic acid. This condition was called the hyperglycemic and hyperlipidemic condition (HHC). Incubation of H9c2 cells in HHC promoted 5.2 times greater total cell death when compared to the control. Of the total death ofthe HHC cells, 38.6% was late apoptotic and 8.3% early apoptotic. HHC also changes cell morphology. The reordering of the actin cytoskeleton and cell stiffness was also studied in control and HHC cells. The actin cytoskeleton was quantified and the number and distance of actin bundles were not the same in the control as under HHC. Young's modulus images show a map of cell stiffness. Cells incubated in HHC with the reordered actin cytoskeleton were stiffer than those incubated in control. The region of greatest stiffness was the peripheral zone of HHC cells (where the number of actin bundles was higher and the distance between them smaller). Our results suggest a correlation between the reordering of the actin cytoskeleton and cell stiffness. Thus, our study showed that HHC can promote morphophysiological changes in rat cardiac cells confirming that gluco-and lipotoxicity may play a central role in the development of diabetic cardiomyopathy.

Diet-Induced Hypercholesterolemia Leads to Cardiac Dysfunction and Alterations in the Myocardial Proteome

“…One of the most notable changes in the level of an individual protein was observed in the case of the downregulated expression of ACTB, an essential component of the non-contractile cytoskeleton system. Similar to our results, metabolic perturbations, such as hyperglycemia and hyperlipidemia, reduced ACTB in both ventricles, which was associated with the further impairment of cellular elasticity and disorganized myocardial actin cytoskeleton [25][26][27]. Furthermore, in our study, MYH6 decreased, and MYH7 increased in the heart as a result of cholesterol feeding.…”

Canagliflozin Delays Aging of HUVECs Induced by Palmitic Acid via the ROS/p38/JNK Pathway

“…In our past study, CAN attenuated cardiomyocyte lipotoxicity through inhibition of the mTOR/HIF-1α pathway, an outcome that, in turn, resulted in the exertion of a protective effect on the diabetic heart [ 45 ]. Recent investigations have verified that lipotoxicity induced by hyperlipidemia or increased blood fatty acid levels can increase fat accumulation and promote vascular aging [ 46 , 47 ]. Aging blood vessels are associated with various cardiovascular diseases.…”

Cardiovascular, Metabolic and Inflammatory Changes after Ovariectomy and Estradiol Substitution in Hereditary Hypertriglyceridemic Rats

“…In contrast to changes of myocardial mass, content of triglycerides in myocardium changed after ovariectomy differently; the content of triglycerides in myocardium was not affected by ovariectomy but it increased significantly if ovariectomy was followed by estradiol substitution even above the values in the sham group. Increased content of triglycerides in heart muscle is recently under investigation and considered to be unfavorable process [ 33 , 34 , 35 ], however, which might be modified [ 36 , 37 ]. In this respect and with respect to findings in other tissues, the favorable effect of estradiol in this case is questionable and it seems that estradiol could cause also unfavorable shifts of fat content between different body compartments [ 37 ], including myocardial tissue.…”