The mechanism of pulmonary hypertension through Cavin family protein

2015 Fiscal Year Final Research Report

• Project/Area Number: 26860579
• Research Category: Grant-in-Aid for Young Scientists (B)
• Allocation Type: Multi-year Fund
• Research Field: Cardiovascular medicine
• Research Institution: Kyoto Prefectural University of Medicine
• Principal Investigator: Nakanishi Naohiko 京都府立医科大学, 医学(系)研究科(研究院), 助教 (10637911)
• Project Period (FY): 2014-04-01 – 2016-03-31
• Keywords: 肺高血圧症 / カベオラ / カベオリン / キャビン

Outline of Final Research Achievements

Emerging evidence suggests that caveolin-1 (Cav1) is associated with pulmonary arterial hypertension. Cavin regulates caveolar formation and functions together with caveolins. We explored the role of Cavin-2/SDPR in the mechanism of the development of pulmonary hypertension (PH).
Cavin-2/SDPR expression was higher in the mouse lung exposed to hypoxia than in that under normoxia. To explore the functional significance of Cavin-2/SDPR in the development of PH, WT and Cavin-2/SDPR knockout mice were exposed to normobaric hypoxia for 4 weeks. After hypoxia, Cavin-2/SDPR knockout mice showed significant aggravation of RVSP elevations and RV hypertrophy compared with wild type mice, suggesting the progression of PH. The phosphorylation of ERK in the lung of Cavin-2/SDPR knockout mice exposed to hypoxia was significantly greater than in the lung of WT mice exposed to hypoxia. These findings suggest the possibility that Cavin-2/SDPR has a role in the development of PH through ERK signaling.

Free Research Field

肺高血圧症