Of cells and tissues: Identifying the elements of a diabetic cardiac in vitro study model.

阅读:2
作者:Hernandez Ivana, Gobinath C, Padilla Andie E, Loyola Carla D, Joddar Binata
This study aimed to elucidate the impact of advanced glycation end products (AGEs) and glucose shock on cardiomyocyte viability, gene expression, cardiac biomarkers, and cardiac contractility. Firstly, AGEs were generated in-house, and their concentration was confirmed using absorbance measurements. AC16 cardiomyocytes were then exposed to varying doses of AGEs, resulting in dose-dependent decreases in cell viability. The maximum tolerated dose of AGEs was determined, revealing significant downregulation of the cardiac gene gap junction alpha 1 (GJA1). Furthermore, the study assessed the effects of AGEs, glucose shock, and their combination on biomarkers, cardiac myosin heavy chain (MHC), and connexin-43 (Cx-43) in AC16 cells. It was found that AGEs supplementation induced an increase in MHC expression while reducing Cx-43 expression, potentially contributing to cardiac dysfunction. Glucose shock also affected cardiomyocyte contractility, highlighting the complex interplay between AGEs, glucose levels, and cardiac function. Additionally, human iPSC-derived cardiomyocytes were subjected to varying doses of AGEs, revealing dose-dependent cytotoxicity and alterations in contractility. Immunostaining confirmed upregulation of MYH7, a cardiac gene associated with muscle contraction, in response to AGEs. However, the expression of Cx-43 was minimal in these cells. This comprehensive investigation sheds light on the intricate relationship between AGEs, glucose shock, and cardiomyocyte function, providing insights into potential mechanisms underlying cardiac dysfunction associated with metabolic disorders such as diabetic cardiomyopathy (DCM).

特别声明

1、本文转载旨在传播信息,不代表本网站观点,亦不对其内容的真实性承担责任。

2、其他媒体、网站或个人若从本网站转载使用,必须保留本网站注明的“来源”,并自行承担包括版权在内的相关法律责任。

3、如作者不希望本文被转载,或需洽谈转载稿费等事宜,请及时与本网站联系。

4、此外,如需投稿,也可通过邮箱info@biocloudy.com与我们取得联系。