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2017 Fiscal Year Final Research Report

Elucidation of the pathomechanism of lung fibrosis from the viewpoint of cellular senescence and cytoskeletal organization

Research Project

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Project/Area Number 16K15460
Research Category

Grant-in-Aid for Challenging Exploratory Research

Allocation TypeMulti-year Fund
Research Field Respiratory organ internal medicine
Research InstitutionUniversity of Miyazaki

Principal Investigator

Nakazato Masamitsu  宮崎大学, 医学部, 教授 (10180267)

Co-Investigator(Kenkyū-buntansha) 柳 重久  宮崎大学, 医学部, 助教 (60404422)
坪内 拡伸  宮崎大学, 医学部, 助教 (60573988)
Project Period (FY) 2016-04-01 – 2018-03-31
Keywords肺線維症 / 肺リモデリング / 細胞老化 / 細胞骨格 / Pten / RhoA / Ror2
Outline of Final Research Achievements

In this study, we investigated the roles of epithelial Pten in the pathogenesis of lung fibrosis by using lung epithelial-specific Pten deficient (Pten-KO) mice. Pten-KO mice showed increased cell senescence and enhanced p53 expressions in alveolar epithelial cells (AECs). Pten-KO mice also showed enhanced cellular senescence-associated secretory phenotype in the lungs, and Pten-KO mice at 30 weeks old showed enhanced lung architectural remodeling (increased mean linear intercept of alveoli and alveolar destruction index). Interestingly, AECs of Pten-KO mice showed impaired bipolar spindle formations. These results indicated that epithelial Pten deficiency causes accelerated cellular senescence of AECs through p53 upregulation and the impairment of bipolar spindle formations, and subsequently enhances lung architectural remodeling.

Free Research Field

呼吸器内科学

URL: 

Published: 2019-03-29  

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