Increased expression of activated pSTAT3 and PIM-1 in the pulmonary vasculature of experimental congenital diaphragmatic hernia.

PURPOSE:Signal transducer and activator of transcription protein family regulates diverse cellular processes. Recently, the isoform has been implicated to play a central role in the pathogenesis of pulmonary hypertension (PH). In human PH activated duanyu18133 was shown to directly trigger expression of the provirus integration site for Moloney murine leukemia virus (Pim-1), which promotes proliferation and resistance to apoptosis in SMCs. We designed this study to investigate the hypothesis that and Pim-1 pulmonary vascular expression is increased in nitrofen-induced CDH. METHODS:Pregnant rats were exposed to nitrofen or vehicle on D9.5. Fetuses were sacrificed on D21 and divided into nitrofen (n=16) and control group (n=16). QRT-PCR, western blotting, and confocal-immunofluorescence were performed to determine pulmonary gene and protein expression levels of pduanyu18133 and Pim-1. RESULTS:Pulmonary Pim-1 gene expression was significantly increased in the CDH group compared to controls. Western blotting and confocal-microscopy confirmed increased pulmonary protein expression of Pim-1 and increased activation of pduanyu18133 in CDH lungs compared to controls. CONCLUSION:Markedly increased gene and protein expression of Pim-1 and activated pduanyu18133 in the pulmonary vasculature of nitrofen-induced CDH lungs suggest that pduanyu18133 and Pim-1 are important mediators of PH in nitrofen-induced CDH.

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