SMOOTH MUSCLE CELL ARACHIDONIC ACID RELEASE, MIGRATION, AND PROLIFERATION

平滑肌细胞花生四烯酸的释放、迁移和增殖

• 批准号: 8168759
• 负责人: Sung K. Moon
• 金额: $ 1.13万
• 依托单位: WASHINGTON UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 2010
• 资助国家: 美国
• 起止时间: 2010-03-10 至 2010-12-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/8168759
• 关键词: Arachidonic Acids; Blood Vessels; Computer Retrieval of Information on Scientific Projects Database; Enzymes; Family; Funding; Grant; Institution; Ionophores; Lipids; Mediating; Mus; Phospholipase A2; Process; Regulation; Research; Research Personnel; Resources; Signal Transduction; Smooth Muscle Myocytes; Source; Thapsigargin; United States National Institutes of Health; member; migration

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Pharmacologic evidence suggests that the lipid products generated by one or more Ca2+-independent phospholipases A2 (iPLA2s) participate in the regulation of vascular tone through smooth muscle cell (SMC) Ca2+ signaling and the release of arachidonic acid. However, the recent identification of new members of the iPLA2 family, each inhibitable by (E)-6-(bromomethyl ene)-3-(1-naphthal enyl )- 2 H- t e t r a hy dr o py r a n- 2 - one, has rendered definitive identification of the specific enzyme(s) mediating these processes difficult. Accordingly, we used iPLA2b-/- mice to demonstrate that iPLA2b is responsible for the majority of thapsigargin and ionophore (A23187)-induced arachidonic acid release from SMCs.

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