Regulation of Orai1 in Angiotensin II-Induced Cardiac Hypertrophy
Refereed conference paper presented and published in conference proceedings


摘要Heart failure initiates with pathological cardiac hypertrophy which is a response of heart to increased workload. The cardiac hypertrophy is characterized as increased cardiomyocytes size, develops during the process of disorders such as hypertension and myocardial infarction. Calcium, as a second messenger, plays vital roles in mediating a wide range of cardiovascular diseases. Few studies reported store operated Ca2+ entry (SOCE) is associated with cardiac hypertrophy yet. Here, we hypothesized Orai1-mediated SOCE is responsible for the Angiotensin II-induced cardiac hypertrophy. Our data showed after the subcutaneous implantation of Ang II osmotic pump in C57BL6 mice, the heart size significantly increased. However, this effect could be abolished by knocking down Orai1 using AAV-Orai1-shRNA. A real-time PCR and western blots results showed the hypertrophic marker genes ANF, BNP, ß-MHC and cTnT upregulated in Ang II treatment group, while they remained nearly unchanged after the treatment of AAV-Orai1-shRNA, indicating Orai1 could rescue the Ang II perfusion induced cardiac hypertrophy in vivo. Moreover, Masson’s Trichrome staining convinced type I collagen levels in heart increased after Angiotensin II perfusion while it is attenuated after blocking Orai1, showing the progress of cardiac fibrosis during Orai1-mediated cardiac hypertrophy. Taken together, these findings suggest Orai1 as a novel regulator involved in Angiotensin II induced cardiac hypertrophy in vivo.
著者Mingxu XIE, Changbo ZHENG, Xiaoqiang YAO
會議名稱The 9th Federation of Asian and Oceanian Physiological Societies Congress (FAOPS2019) in conjunction with the 96th Annual Meeting of the Physiological Society of Japan
會議地點Kobe Convention Center, Kobe, Japan

上次更新時間 2019-03-05 於 16:29