Evidence is growing that PPARγ could improve the bioavailability of NO in pathological conditions to maintain endothelial function by activating Akt/eNOS pathway. LincRNAs participate in regulating development of cardiovascular diseases. Although investigations have been made to delineate the function of PPARγ and lincRNAs, little is known about the regulation relationship between them, especially in endothelial cells. In this study, we not only verified that PPARγ could antagonize the adverse effects brought from ox-LDL, but also found a novel factor related to PPARγ, named linc01230. According to our study, PPARγ transcriptionally regulated linc01230 by specifically combining with two binding regions, which have superposition effect, in the upstream of linc01230 promoter. In addition, linc01230 reduced ox-LDL induced endothelial dysfunction and affected the phosphorylation of Akt. These results conclude linc01230 as a novel modifier in PPARγ-mediated activation of Akt in endothelial function.
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