Alternative Title心房組織の静水圧負荷はTGF-βシグナル経路を介して線維化促進転写を活性化する
Periodical titleInternational Heart Journal
Degree grantor/typeNagasaki University (長崎大学)
Note (General)Excessive mechanical stress causes fibrosis-related atrial arrhythmia. Herein, we tried to investigate the mechanism of atrial fibrogenesis in response to mechanical stress by ex vivo approach. We collected atrial tissues from mice and then cultured them as "explants" under atmospheric pressure (AP group) or 50 mmHg hydrostatic pressure loading (HP group) conditions. Pathway-specific PCR array analysis on the expression of fibrosis-related genes indicated that the loading of atrial tissues to 50 mmHg for 24 hours extensively upregulated a series of profibrotic genes. qRT-PCR data also showed that loading atrial tissues to 50 mmHg enhanced Rhoa, Rock2, and Thbs1 expression at different time points. Interestingly, the enhanced expression of Thbs1 at 1 hour declined at 6-24 hours and then increased again at 72 hours. In contrast, an enhanced expression of Tgfb1 was observed at 72 hours. In contrast, daily loading to 50 mmHg for 3 hours significantly accelerated the outgrowth of mesenchymal stem-like stromal cells from atrial tissues; however, we did not observe significant phenotypic changes in these outgrowing cells. Our ex vivo experimental data clearly show the induction of profibrotic transcription of atrial tissues by HP loading, which confirms the common pathological feature of atrial fibrosis following pressure overload.
長崎大学学位論文 学位記番号:博(医歯薬)甲第1446号 学位授与年月日:令和4年3月18日
Author: Xu Zhang, Yousuf Yassouf, Kai Huang, Yong Xu, Zi-Sheng Huang, Da Zhai, Reiko Sekiya, Ke-Xiang Liu, Tao-Sheng Li
Citation: International Heart Journal, 63(2), pp. 367-374; 2022
identifier:Nagasaki University (長崎大学), 博士(医学) (2022-03-18)
http://hdl.handle.net/10069/00041449
Collection (particular)国立国会図書館デジタルコレクション > デジタル化資料 > 博士論文
Date Accepted (W3CDTF)2022-07-05T02:30:21+09:00
Data Provider (Database)国立国会図書館 : 国立国会図書館デジタルコレクション