cyclin-d1 and Hepatopulmonary-Syndrome

cyclin-d1 has been researched along with Hepatopulmonary-Syndrome* in 1 studies

Other Studies

1 other study(ies) available for cyclin-d1 and Hepatopulmonary-Syndrome

Article	Year
The ET-1-mediated carbonylation and degradation of ANXA1 induce inflammatory phenotype and proliferation of pulmonary artery smooth muscle cells in HPS. PloS one, 2017, Volume: 12, Issue:4 Hepatopulmonary syndrome (HPS) is a serious complication of advanced liver disease, which markedly increases mortality. Pulmonary vascular remodelling (PVR) induced by circulating mediators plays an important role in the pathogenesis of HPS, while the underlying mechanism remains undefined. In the present study, we reported that endothelin-1 (ET-1) is up-regulated and annexin A1(ANXA1) is down-regulated in HPS rat, and ET-1 decreases the ANXA1 expression in a dose-dependent manner in rat pulmonary arterial smooth muscle cells (PASMCs). Then, we showed that ANXA1 can decrease nuclear p-ERK1/2 accumulation and decrease the cyclin D1 expression, thus resulting in the subsequent inhibition of PASMCs proliferation. As previously reported, we confirmed that ET-1 decreases the ANXA1 protein levels by the carbonylation and degradation of ANXA1. In conclusion, our research links the signaling cascade of ET1-ANXA1-cell proliferation to a potential therapeutic strategy for blocking IPS-associated PVR. Topics: Animals; Annexin A1; Cell Proliferation; Cells, Cultured; Cyclin D1; Down-Regulation; Endothelin-1; Hepatopulmonary Syndrome; Inflammation; MAP Kinase Signaling System; Muscle, Smooth, Vascular; Myocytes, Smooth Muscle; Phenotype; Protein Carbonylation; Pulmonary Artery; Rats; Rats, Sprague-Dawley; Signal Transduction; Up-Regulation	2017

Article

Year

The ET-1-mediated carbonylation and degradation of ANXA1 induce inflammatory phenotype and proliferation of pulmonary artery smooth muscle cells in HPS.

PloS one, 2017, Volume: 12, Issue:4

Hepatopulmonary syndrome (HPS) is a serious complication of advanced liver disease, which markedly increases mortality. Pulmonary vascular remodelling (PVR) induced by circulating mediators plays an important role in the pathogenesis of HPS, while the underlying mechanism remains undefined. In the present study, we reported that endothelin-1 (ET-1) is up-regulated and annexin A1(ANXA1) is down-regulated in HPS rat, and ET-1 decreases the ANXA1 expression in a dose-dependent manner in rat pulmonary arterial smooth muscle cells (PASMCs). Then, we showed that ANXA1 can decrease nuclear p-ERK1/2 accumulation and decrease the cyclin D1 expression, thus resulting in the subsequent inhibition of PASMCs proliferation. As previously reported, we confirmed that ET-1 decreases the ANXA1 protein levels by the carbonylation and degradation of ANXA1. In conclusion, our research links the signaling cascade of ET1-ANXA1-cell proliferation to a potential therapeutic strategy for blocking IPS-associated PVR.

Topics: Animals; Annexin A1; Cell Proliferation; Cells, Cultured; Cyclin D1; Down-Regulation; Endothelin-1; Hepatopulmonary Syndrome; Inflammation; MAP Kinase Signaling System; Muscle, Smooth, Vascular; Myocytes, Smooth Muscle; Phenotype; Protein Carbonylation; Pulmonary Artery; Rats; Rats, Sprague-Dawley; Signal Transduction; Up-Regulation

2017