Circulatory microRNA expression profile for coronary artery calcification in chronic kidney disease patients.

BACKGROUND & AIM: Coronary artery disease (CAD) is the primary cause of mortality in patients with end stage renal disease (ESRD). MicroRNA profiling is proven as a powerful tool in the diagnosis of any disease at the molecular level. Hence, the present study aimed to profile the microRNA expression for CAD especially coronary artery calcification in CKD patients. MATERIALS AND METHODS: Two hundread patients with CKD stages 3 to 5 without dialysis and healthy controls were included in this study. All two hundred patients underwent 1024 multi sliceardiac computed tomography (CT) scan for calcium scoring. The calcium scoring more than 100 have been included in the study. We performed miRNA microarray analysis from serum samples of seven high calcium scored with CKD patients and one control patients. RESULTS: Seven patients have observed circulating miRNAs has significantly upregulated and downregulated when compared with control patients. mir21, mir 67, mir 390, mir 56, mir 250, mir 65 and mir 13 were up regulated and mir235, mir256, mir226, mir207, mir255, mir193 were downregulated. There was no significant difference in left ventricle function. CONCLUSION: 13 microRNAs play a potential role in coronary artery calcification in CKD patients.

Parthenolide induces apoptosis and autophagy through the suppression of PI3K/Akt signaling pathway in cervical cancer.

OBJECTIVE: To investigate the effect of parthenolide on apoptosis and autophagy and to study the role of the PI3K/Akt signaling pathway in cervical cancer. RESULTS: Parthenolide inhibits HeLa cell viability in a dose dependent-manner and was confirmed by MTT assay. Parthenolide (6 µM) induces mitochondrial-mediated apoptosis and autophagy by activation of caspase-3, upregulation of Bax, Beclin-1, ATG5, ATG3 and down-regulation of Bcl-2 and mTOR. Parthenolide also inhibits PI3K and Akt expression through activation of PTEN expression. Moreover, parthenolide induces generation of reactive oxygen species that leads to the loss of mitochondrial membrane potential. CONCLUSION: Parthenolide induces apoptosis and autophagy-mediated growth inhibition in HeLa cells by suppressing the PI3K/Akt signaling pathway and mitochondrial membrane depolarization and ROS generation. Parthenolide may be a potential therapeutic agent for the treatment of cervical cancer.