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.

我们发现二型三磷酸肌醇受体是细胞内钙释放通道之一，在肺组织中特异性地表达于肺血管的血管平滑肌细胞，而不是全身动脉和肺组织中的支气管，并且二型三磷酸肌醇受体基因的缺失可能会加重野百合碱吡咯所致的肺动脉高压。我们的结果提示，2型三磷酸肌醇受体可能具有控制肺血管张力和负性调节肺动脉高压加重的作用。