Rapid atrial pacing induces myocardial fibrosis by down-regulating Smad7 via microRNA-21 in rabbit

• DOI: 10.1007/s00380-016-0808-z
• Publication Date: 2016-03-11T08:17:49Z
• Authors: Xuyu He; Kunyi Zhang; Xiuren Gao; Liwen Li; Hong Tan; Jiyan Chen; Yingling Zhou
• Keywords: Myocardial fibrosis; Cardiac Fibrosis

Tachycardia-induced atrial fibrosis is a hallmark of the structural remodeling fibrillation (AF). The mechanisms underlying tachycardia-induced remain unclear. In our previous study, we found that Smad7-downregulation promoted development in AF. Fibroblasts are enriched microRNA-21 (miR-21), which contributes to and heart failure cardiovascular system. Our study was designed test hypothesis miR-21 reinforces TGF-β1/Smad signaling pathway AF-induced by down-regulating Smad7. Rapid pacing (RAP, 1000 ppm) applied left atrium rabbit induce fibrosis. qRT-PCR northern blot analysis revealed RAP caused marked increase expression miR-21. Transfection with inhibitor significantly increased Smad7, while collagen I/III decreased. These changes were implicated release down-regulation Adult rat cardiac fibroblasts treated TGF-β1 showed decreased Smad7 expression. Pretreatment reduced TGF-β1-induced up-regulation pre-miR-21 expression, respectively. This result negatively correlated fibroblasts. Moreover, results luciferase activity assay suggest validated target CFs. provide compelling evidence specific degradation may decrease inhibitory feedback regulation serves as new insight mechanism fibrillation.