ABSTRACT
Lysophosphatidic acid(LPA)is a small bioactive phospholipid that mediates various cellular processes such as proliferation, survival, and migration. In particular, LPA signaling has been shown to affect the development of diverse tissues. Our previous work demonstrated that LPA could promote primary neonatal rat cardiomyocytes proliferation. However, the role of LPA and its receptor in postnatal heart de-velopment is unknown. By using databases for biological information and RT-qPCR, we analyzed the ex-pression of six LPA receptors (LPA
ABSTRACT
<p><b>OBJECTIVE</b>To investigated the effect of lovastatin on hypoxia and serum deprivation (Hypoxia/SD) induced rat MSCs apoptosis in vitro and associated signaling pathway changes.</p><p><b>METHODS</b>MSCs were isolated from Sprague-Dawley rats. The anti-apoptotic effects of lovastatin were detected using Hoechst33342 and annexin V-FITC/PI binding assay by Flow cytometric analysis. The phosphorylation of Akt and ERK1/2, the cytochrome C and the cleaved caspase-3 were detected by Western blot.</p><p><b>RESULTS</b>Lovastatin (0.01 - 1 micromol/L) significantly reduced Hypoxia/SD-induced MSCs apoptosis and increased Akt phosphorylation, reduced caspase-3 activation and cytochrome c release from mitochondria to cytosol in a time dependent manner. These effects could be significantly blocked by both PI3K inhibitor, LY294002 and ERK1/2 inhibitor, U0126.</p><p><b>CONCLUSIONS</b>Our results showed that lovastatin protects MSCs from Hypoxia/SD-induced apoptosis via activating PI3K/Akt and ERK1/2 signaling pathways suggesting a potential role of statins as an adjunct therapeutic agent during transplanting MSCs into damaged heart after myocardial infarction.</p>