GROWTH FACTOR CONTROL OF APOPTOSIS DURING PLACENTATION

植入期间细胞凋亡的生长因子控制

• 批准号: 6182050
• 负责人: Sohaib A. Khan
• 金额: $ 20.89万
• 依托单位: UNIVERSITY OF CINCINNATI
• 依托单位国家: 美国
• 财政年份: 1994
• 资助国家: 美国
• 起止时间: 1994-04-01 至 2004-03-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/6182050
• 关键词: BCL2 gene /protein; apoptosis; cathepsin D; cell differentiation; cell growth regulation; cell line; confocal scanning microscopy; cysteine endopeptidases; cytochrome c; decidua; embryo implantation; endometrium; estrogens; gene expression; growth factor receptors; hormone regulation /control mechanism; immunoelectron microscopy; immunoprecipitation; in situ hybridization; laboratory rat; progesterone; receptor binding; transforming growth factors; western blottings; yeast two hybrid system

DESCRIPTION: (Adapted from applicant's abstract) The studies proposed in this application will: (1) determine if progesterone withdrawal at different stages of decidualization would affect the expression of bcl-2 gene family members; this information will be correlated with DNA fragmentation in the decidual cells; (2) investigate why induced Bax expression failed to cause death of decidual cells by determining if Bax activity is compromised by Bcl-xL or hsp-25; (3) determine the expression of TGF-beta and apoptotic mediators (cathepsin-D, cytochrome- c, apaf-1, and caspase-3) in the GG-AD decidual cell line, and assess the consequence of overexpressing bax or inhibiting bax and cathepsin-D in GG-AD cells.

描述：（改编自申请人摘要）拟定研究 在本申请中将：（1）确定是否在 蜕膜化的不同阶段影响bcl-2的表达 基因家族成员;这些信息将与DNA （2）探讨Bax诱导的原因 通过确定Bax是否能引起蜕膜细胞死亡， 活性被Bcl-xL或hsp-25损害;（3）确定 TGF-β和凋亡介质（组织蛋白酶-D，细胞色素-D）的表达， c、apaf-1和caspase-3）在GG-AD蜕膜细胞系中的表达，并评估 过度表达bax或抑制bax和组织蛋白酶-D结果 在GG-AD细胞中。