Analysis of microenvironment and exploration of new biomarker for pulmonary arterial hypertention

2017 Fiscal Year Final Research Report

• Project/Area Number: 15K08359
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: Human pathology
• Research Institution: Hokkaido University
• Principal Investigator: Tanino Mishie 北海道大学, 医学研究院, 講師 (90360908)
• Co-Investigator(Kenkyū-buntansha): 辻野 一三 北海道大学, 医学研究院, 特任教授 (00344507) ; 仙葉 愼吾 北海道大学, 医学研究院, 学術研究員 (40466496) ; 谷野 功典 福島県立医科大学, 医学部, 准教授 (10443863)
• Project Period (FY): 2015-04-01 – 2018-03-31
• Keywords: 肺高血圧 / ニース分類 / 免疫組織化学染色 / 遺伝子解析

Outline of Final Research Achievements

(1)Immunohistochemisty for FGFR1, VEGFR2, EGFR in the lungs of pulmonary venous obstructive hypertension(PVOD) showed higher expression of FGFR compared to VEGFR and EGFR in PVOD lungs. FGF-FGFR may pathway contribute the pathogenesis of PVOD. (2)Therapy related proteins such as PDE5、ER-A/B、PGI2、sGCα/βexpressed higher in pulmonary hypertension(PH) compared to controls, however there were no difference between Group 1-PH and Group 3-PH. These drugs contribute to dilate vessel wall in both types of PH. (3) Systemic sclerosis (Ssc) related PH showed denser fibrosis compared to SLE related PH and replacement myocardial fibrosis was demonstrated at the site of late gadolinium enchancement of MRI in Ssc patient.(4) FoxF1 mutation was detected in Alveolar capillary dysplasia related PH children and Heterozygous mutations in OAS1 were detected in infantile-onset pulmonary alveolar proteinosis with hypogammaglobulinemia. These genetic background relate to secondary PH.

Free Research Field

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