miR-873 suppresses H9C2 cardiomyocyte proliferation by targeting GLI1.

MicroRNAs (miRNAs) are a class of endogenous, non-coding small RNAs that regulate the expression of target genes. Previous studies have suggested that miRNAs are key regulators in cardiovascular systems. This study investigated the role of miR-873 in H9C2 cardiomyocytes by targeting glioma-associated oncogene 1 (GLI1). miR-873 was significantly up-regulated in serum samples from congenital heart disease (CHD) patients compared with those from normal individuals. Furthermore, miR-873 over-expression suppressed H9C2 proliferation and induced cell cycle arrest. Bioinformatic algorithms revealed a predicted target site for miR-873 in the 3'-untranslated region (3'UTR) of GLI1, which was verified using a dual-luciferase reporter assay. qPCR and western blot analysis also showed that miR-873 negatively regulated GLI1 mRNA and protein expression in H9C2 cells. Conversely, GLI1 over-expression partially reversed the growth-inhibitory effect of miR-873. To summarize, our data suggest that miR-873 is a novel miRNA that regulates H9C2 cell proliferation via targeting GLI1, and miR-873 may serve as a new potential biomarker diagnosis in CHD in the future.

Role of platelet derived growth factor (PDGF) in reverting neuronal nuclear and soma size alterations in NSC-34 cells exposed to cerebrospinal fluid from amyotrophic lateral sclerosis patients.

PURPOSE: Amyotrophic lateral sclerosis (ALS) or motor neuron disease is an adult-onset progressive neurodegenerative disorder. ALS-CSF has been shown to produce toxic effects on motor neuron cells like aberrant neurofilament phosphorylation and morphological alterations of nuclear and soma size. Our current study was designed to investigate the neuroprotective role of platelet derived growth factor (PDGF) in reverting the adverse effects produced by ALS-CSF. METHODS: Our present study was carried out to determine the restorative potential of PDGF on the toxic effects of ALS-CSF on NSC motor neuron cells from patients. Therefore the cells were divided in to three groups: (a) normal control (NC) - the cells were not exposed to ALS-CSF; (b) ALS group - the cells were exposed to ALS-CSF; (c) NALS group - the cells were exposed to non ALS CSF. Further each of these groups was supplemented with PDGF. RESULTS AND CONCLUSIONS: We observed that the mean area of nucleus and cell soma of the differentiated NSC motor neuron cells was significantly reduced in the cells exposed to ALS-CSF. We also observed that subsequent treatment with PDGF restored the soma area and nucleus of the ALS-CSF exposed cells significantly. Taken together, we show that supplementation with PDGF restores the morphological changes induced by ALS-CSF and PDGF may play a significant role in protecting motor neurons from apoptosis in ALS and thereby it promoting the cell survival.