Atherosclerotic cardiovascular disease and acute myocardial infarction are the leading causes of mortality worldwide, and apoptosis is the major pathway of cardiomyocyte death under hypoxic conditions. Although studies have reported changes in the expression of certain pro-apoptotic and anti-apoptotic genes in hypoxic cardiomyocytes, genetic regulations are complex in human cardiomyocytes and there is much that remains to be fully elucidated. The present study aimed to identify differentially expressed genes in hypoxic human AC16 cardiomyocytes using next-generation sequencing and bioinformatics. A total of 24 genes (15 upregulated and 9 downregulated) with potential micro (mi)RNA-mRNA interactions were identified in the miRmap database. Utilising the Gene Expression Omnibus database of cardiac microvascular endothelial cells, tensin 1, B-cell lymphoma 2-interacting protein 3 like, and stanniocalcin 1 were found to be upregulated, and transferrin receptor and methyltransferase like 7A were found to be downregulated in response to hypoxia. Considering the results from miRmap, TargetScan and miRDB together, two potential miRNA-mRNA interactions were identified: hsa-miRNA (miR)-129-5p/CDC42EP3 and hsa-miR-330-3p/HELZ. These findings contribute important insights into possible novel diagnostic or therapeutic strategies for targeting cardiomyocytes under acute hypoxic stress in conditions, including acute myocardial infarction. The results of the present study also introduce an important novel approach in investigating acute hypoxic pathophysiology.

The road to drug discovery for heart‐related diseases is challenged by advancement in whole‐heart and reliable animal heart models. In vitro model is a solution to replacing the unpredictable in vivo heart models. However, the techniques are time‐ and cost‐consuming. Cardiomyocyte cell line that expands in culture can be trained by mechanical stimulation to express cardiac biomarkers. The use of mechanical stimulation such as cyclic stretching can be more predictable, reliable in terms of cardiac marker expressions. The heart is an organ that is in constant dynamic which requires regulation for reactive oxygen species (ROS) to prevent pathological process. Here, we used cyclic stretching to stimulate cardiomyocytes with mild (5%), and aggressive (25%) strains at 1Hz. The stimulated cardiomyocytes expressed the cardiac characteristic markers Atrial natriuretic factor (ANF), and β‐myosin heavy chain (β‐MHC) after 24h of stretching. The 3H‐1,2‐dithiole‐3‐thione (D3T) has been reported to be a potent inducer of antioxidant genes through activation of the transcription factor Nrf2, and Nrf2 has been reported to play a role in cardiac remodeling.In this study, we investigated the effect of the D3T on the cardiomyocytes stimulated at mild, or aggressive strain. Results show that the aggressive strain reduced the β‐MHC expression, and the D3T enhanced the β‐MHC expression in cardiomyocytes that were stimulated with aggressive strain.Support or Funding InformationThis research is supported by VGHKS107‐076, VGHKS107‐168, VGHKS107‐175, MOST104‐2320‐B‐0751B‐003‐MY3, and MOST106‐2320‐B‐075B‐001.This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.