and Are Affected by Stretch in HL-1 Atrial Myocytes.

Background: Lipid expression is increased in the atrial myocytes of mitral regurgitation (MR) patients. This study aimed to investigate key regulatory genes and mechanisms of atrial lipotoxic myopathy in MR.

Methods: The HL-1 atrial myocytes were subjected to uniaxial cyclic stretching for eight hours. Fatty acid metabolism, lipoprotein signaling, and cholesterol metabolism were analyzed by PCR assay (168 genes).

Results: The stretched myocytes had significantly larger cell size and higher lipid expression than non-stretched myocytes (all < 0.001). Fatty acid metabolism, lipoprotein signaling, and cholesterol metabolism in the myocytes were analyzed by PCR assay (168 genes). In comparison with their counterparts in non-stretched myocytes, seven genes in stretched monocytes (, , , , , , ) revealed differential upregulation with an altered fold change >1.5. Nine genes in stretched monocytes (, , , , , , , , ) revealed differential downregulation with an altered fold change <0.67. Canonical pathway analysis, using Ingenuity Pathway Analysis software, revealed that the only genes in the "superpathway of cholesterol biosynthesis" were (upregulated) and (downregulated). The fraction of stretched myocytes expressing Nile red was significantly decreased by RNA interference of ( < 0.05) and was significantly decreased by plasmid transfection of ( = 0.004).

Conclusions: The and genes have regulatory roles in atrial lipotoxic myopathy associated with atrial enlargement.