molecular signaling mechanism via IP3 receptors in vascular endothelial cells in a state of pulmonary hypertension

肺动脉高压状态下血管内皮细胞IP3受体的分子信号传导机制

• 批准号: 22791000
• 负责人: KODO Kazuki
• 金额: $ 2.5万
• 依托单位: Keio University
• 依托单位国家: 日本
• 项目类别: Grant-in-Aid for Young Scientists (B)
• 财政年份: 2010
• 资助国家: 日本
• 起止时间: 2010 至 2011
• 项目状态: 已结题
• 来源: https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-22791000/
• 关键词: 小児循環器学; 肺高血圧; IP3受容体; 肺血管内皮; 肺血管平滑筋; VEGF; エンドセリン; モノクロタリン

We have found that type 2 inositol trisphosphate receptor, one of intracellular calcium release channels, is expressed specifically in the vascular smooth muscle cells of the pulmonary arteries not of the systemic arteries nor of the bronchi in the lung tissue, and that disruption of the gene of type 2 inositol trisphosphate receptor might worsen monocrotaline pyrrole-induced pulmonary hypertension. Our results suggest that type 2 inositol trisphosphate receptor might have a role for controlling pulmonary vascular tone and negatively regulate exacerbation of pulmonary hypertension.

我们已经发现，2型2型肌醇三磷酸受体（细胞内钙释放通道之一）在肺动脉的肺动脉的血管平滑肌细胞中特别表达，而不是全身性动脉或支气管中的支气管中的支气管，肺组织中的支气管造成了2型内醇三磷酸三磷酸三磷酸型塑料的基因的破坏高血压。我们的结果表明，2型肌醇三磷酸受体可能在控制肺血管张力和负调节肺动脉高压加剧的情况下起作用。

项目成果

A Decade of Advances in the Molecular Embryology and Genetics Underlying Congenital Heart Defects

• DOI: 10.1253/circj.cj-11-0636
• 发表时间: 2011-10-01
• 期刊: CIRCULATION JOURNAL
• 影响因子: 3.3
• 作者: Kodo, Kazuki;Yamagishi, Hiroyuki
• 通讯作者: Yamagishi, Hiroyuki