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APOPTOSIS IN PULMONARY FIBROSIS

APOPTOSIS IN PULMONARY FIBROSIS
肺纤维化中的细胞凋亡
批准号：
2658170
负责人：
David J. McConkey
金额：
$7.35万
依托单位：
UNIVERSITY OF TX MD ANDERSON CAN CTR
依托单位国家：
美国
项目类别：
财政年份：
1997
资助国家：
美国
项目状态：
已结题
起止时间：
1997-09-30 至 1999-08-31
来源：
https://reporter.nih.gov/project-details/2658170
关键词：
apoptosis bleomycin cytokine drug adverse effect gene targeting genetically modified animals inflammation interleukin 1 laboratory mouse macrophage oxidative stress pulmonary fibrosis /granuloma respiratory airway clearance tumor suppressor genes tumor suppressor proteins

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DESCRIPTION The proposal is designed to establish how oxidative stress caused by bleomycin treatment leads to macrophage apoptosis and lung fibrosis. The investigators postulate that this apoptotic response causes impaired clearance of lung debris and release of inflammatory cytokines, particularly IL1 beta. They present three specific aims to test the hypothesis. Aim 1 is an in vitro study using peritoneal macrophages to determine the involvement of oxidative stress in bleomycin-induced apoptosis. The second aim is an in vivo study using p53 knockout animals to test the role of this protein in apoptosis and concomitant bleomycin-induced fibrosis. Third is to define the role of IL1 beta and interleukin converting enzymes in lung fibrosis.
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