Platelet activation receptor CLEC-2: The role for lung development.

2014 Fiscal Year Final Research Report

• Project/Area Number: 23590330
• Research Category: Grant-in-Aid for Scientific Research (C)
• Allocation Type: Multi-year Fund
• Section: 一般
• Research Field: General medical chemistry
• Research Institution: University of Yamanashi
• Principal Investigator: INOUE Osamu 山梨大学, 総合研究部, 准教授 (00432154)
• Co-Investigator(Renkei-kenkyūsha): INOUE Katsue (SUZUKI Katsue) 山梨大学, 総合研究部, 准教授 (10324211) ; TSUKIJI Nagaharu 山梨大学, 総合研究部, 助教 (20710362)
• Project Period (FY): 2011-04-28 – 2015-03-31
• Keywords: CLEC-2 / 血小板 / 肺 / 発生 / myofibroblast

Outline of Final Research Achievements

The mice deficient in CLEC-2 die just after birth. We found that the newborn mice deficient in CLEC-2 have severe abnormalities in lung structure, and these neonates also have abnormalities in the distribution of myofibroblasts in lung. The conditional knockouts that do not express CLEC-2 on platelets also have these abnormalities in lung, indicating that the CLEC-2 on platelets, but not the CLEC-2 on other hematocytes plays a role in lung development. In vitro study, we confirmed that the granule contents secreted by platelets upon activation facilitate a development of myofibroblasts from lung mesothelial cells. In this study, we clarified the novel mechanism that blood platelets regulate the development of lung through the C-type lectin-like receptor, CLEC-2.

Free Research Field

血小板生物学