LIPID CONTROL IN THE REMOVAL OF DYING BRAIN TUMOR CELLS

去除垂死脑肿瘤细胞时的脂质控制

• 批准号: 2611440
• 负责人: RUTH E. STARK
• 金额: $ 11.36万
• 依托单位: COLLEGE OF STATEN ISLAND
• 依托单位国家: 美国
• 财政年份: 1998
• 资助国家: 美国
• 起止时间: 1998-05-01 至 2001-04-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/2611440
• 关键词: antisense nucleic acid; apoptosis; brain neoplasms; cell line; enzyme inhibitors; gas chromatography mass spectrometry; hypoxia; liposomes; membrane activity; membrane lipids; microglia; neoplastic cell; neuroblastoma; phagocytosis; phosphatidylserines; phospholipids; saturated fatty acids; serotonin receptor; transfection

DESCRIPTION: Apoptosis (or programmed cell death) is not completely understood The applicant's group has shown that apoptosis in the malignant neuronal HN2-5 cell line is associated with an increase in saturated fatty acid- phospholipid which increase membrane rigidity and with the expression of serotonin 1A receptor (5-HT1A -R). The applicant postulates that a change in membrane lipid composition inhibits such membrane-bound enzymes as aminophospholipid translocase (APTL) which helps to localize phosphatidylserine (PS) to the inne membrane leaflet. The redistribution of PS to the outer leaflet during apoptosis appears to be a dominant signal to trigger phagocytosis of apoptotic cells by microglia. The overall goals of this program are 1) to understand wha changes in membrane lipid composition occur in HN2-5 cells during apoptosis an 2) to determine how these changes affect phagocytosis of apoptotic cells by th microglia. The applicant proposes studies that will either mimic the phospholipid membrane changes or reproduce them in a controlled manner. He wil also attempt to induce some of the phospholipid changes while maintaining the viability of the tumor cells. This project will help provide an understanding of some of the membrane alterations that occur during apoptosis.

描述：凋亡（或程序性细胞死亡）并非完全 了解申请人的群体表明恶性肿瘤的凋亡 神经元HN2-5细胞系与饱和脂肪的增加有关 酸性磷脂，增加膜刚度和表达 5-羟色胺1A受体（5 -HT1A -R）的含量。 申请人假设 膜脂质组成的变化抑制了这种结合膜结合的酶 氨基磷脂易位酶（APTL），有助于本地化 磷脂酰丝氨酸（PS）到Inne膜小叶。 重新分布 凋亡过程中对外部小叶的PS似乎是主要信号 触发小胶质细胞对凋亡细胞的吞噬作用。 总体目标 该程序是1）了解膜脂质成分的变化 在凋亡过程中发生在HN2-5细胞中2）确定这些改变 影响小胶质细胞对凋亡细胞的吞噬作用。 申请人 提出的研究将模仿磷脂膜变化或 以受控的方式重现它们。 他还试图诱导一些 磷脂的变化，同时保持肿瘤的生存能力 细胞。 该项目将有助于了解一些 凋亡过程中发生的膜改变。