Wei Zhang
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Research Interests
Wei Zhang has a total of 7 co-authors. Here are the top co-authors by number of shared publications:
Haifang Rong
Department of Respiratory, The First Hospital of Harbin, Harbin, Heilongjiang 150000, P.R. China
1 shared publicationLiguo Wang
Department of Respiratory, First Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang 150000, P.R. China
1 shared publicationLiwei Zhuang
Department of Gastroenterology, The Fourth Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang 150000, P.R. China
1 shared publicationRuifeng Wang
Department of Gastroenterology, The Fourth Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang 150000, P.R. China
1 shared publicationXiaohua Ling
Department of Gastroenterology, The Fourth Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang 150000, P.R. China
1 shared publicationXin Yu
Department of Gastroenterology, The Fourth Affiliated Hospital of Harbin Medical University, Harbin, Heilongjiang 150000, P.R. China
1 shared publication
Latest Publications
- Open Access
- 22 October 2012
- Published by Spandidos Publications in Molecular Medicine Reports
- Vol. 12 (6) , 8261-8267
MicroRNA-101 inhibits proliferation of pulmonary microvascular endothelial cells in a rat model of hepatopulmonary syndrome by targeting the JAK2/STAT3 signaling pathway
Hepatopulmonary syndrome (HPS) is one of the reasons for the mortality of patients with perioperative liver disease. Intrapulmonary vascular dilatation is the most important mechanism underlying HPS, and it primarily occurs due to cell proliferation. Inhibiting the proliferation of pulmonary microvascular endothelial cells (PMVECs) may provide a novel strategy to prevent HPS. MicroRNAs (miRNAs) regulate gene expression and are crucial in cell proliferation. To investigate the mechanism underlying the proliferation of PMVECs in HPS, PMVECs were isolated from rat models of HPS. It was demonstrated that interleukin (IL)‑6 could stimulate the janus kinase 2 (JAK2)/ signal transducer and activator of transcription (STAT3) signaling pathway, which promotes the cell proliferation of PMVECs. JAK2 is a novel target gene of miR-101 and it was shown that miR-101 could inhibit cell proliferation by targeting the IL-6/JAK2/STAT3 signal pathway. In conclusion, the present study demonstrated that miR-101 could inhibit the proliferation of PMVECs by targeting the IL-6/JAK2/STAT3 signaling pathway. This clarifies the role of miR-101 in HPS and provides the theoretical basis of the pathogenesis of HPS.
- 22 October 2012
- Published by Spandidos Publications in Molecular Medicine Reports
- Vol. 12 (6) , 8261-8267
Open AccessMicroRNA-101 inhibits proliferation of pulmonary microvascular endothelial cells in a rat model of hepatopulmonary syndrome by targeting the JAK2/STAT3 signaling pathway
Hepatopulmonary syndrome (HPS) is one of the reasons for the mortality of patients with perioperative liver disease. Intrapulmonary vascular dilatation is the most important mechanism underlying HPS, and it primarily occurs due to cell proliferation. Inhibiting the proliferation of pulmonary microvascular endothelial cells (PMVECs) may provide a novel strategy to prevent HPS. MicroRNAs (miRNAs) regulate gene expression and are crucial in cell proliferation. To investigate the mechanism underlying the proliferation of PMVECs in HPS, PMVECs were isolated from rat models of HPS. It was demonstrated that interleukin (IL)‑6 could stimulate the janus kinase 2 (JAK2)/ signal transducer and activator of transcription (STAT3) signaling pathway, which promotes the cell proliferation of PMVECs. JAK2 is a novel target gene of miR-101 and it was shown that miR-101 could inhibit cell proliferation by targeting the IL-6/JAK2/STAT3 signal pathway. In conclusion, the present study demonstrated that miR-101 could inhibit the proliferation of PMVECs by targeting the IL-6/JAK2/STAT3 signaling pathway. This clarifies the role of miR-101 in HPS and provides the theoretical basis of the pathogenesis of HPS.