MicroRNA-135a inhibits cardiac fibrosis induced by isoproterenol via TRPM7 channel - 11/06/18
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Graphical abstract |
Highlights |
• | Silencing of TRPM7 decreased collagen I and α-SMA expressions in CFs. |
• | Overexpression of miR-135a inhibits ISO-induced CFs proliferation and differentiation. |
• | TRPM7 is one of the targets of miR-135a. |
• | MiR-135a protected against ISO-induced cardiac fibrosis via TRPM7 channel. |
Abstract |
Background |
Cardiac fibrosis is a crucial factor of heart failure. It has been reported that several microRNAs (miRNAs, miRs) were involved in cardiac fibrosis, however, the role and possible regulatory mechanism of microRNA-135a (miR-135a) in cardiac fibrosis have not been investigated. Here, we explored the regulation mechanism of miR-135a on cardiac fibrosis.
Methods and Results |
In vitro, cardiac fibroblasts (CFs) from neonatal rats were treated by isoproterenol (ISO) at the final concentration of 10 μM for 24 h and miR-135a expression was decreased obviously. A miR-135a mimic inhibited CFs proliferation and differentiation by down-regulating transient receptor potential melastatin 7 (TRPM7) expression and current, whose effects were reversed by either the addition of miR-135a mimic or silencing TRPM7. In vivo, adult SD rat cardiac fibrosis was induced by subcutaneous administration of ISO (5 mg/kg/day) for 10 days. The expression of Collagen I, α-smooth muscle actin (α-SMA) and TRPM7 were up-regulated while miR-135a was down-regulated. In summary, our results illustrated that TRPM7 channel played an essential role in regulating fibrosis and that miR-135a protected against ISO-induced cardiac fibrosis via TRPM7 channel.
Conclusion |
MiR-135a inhibits cardiac fibrosis via miR-135a- TRPM7-collagen production pathway.
Le texte complet de cet article est disponible en PDF.Keywords : miR-135a, Isoproterenol, TRPM7, Cardiac fibrosis
Plan
Vol 104
P. 252-260 - août 2018 Retour au numéroBienvenue sur EM-consulte, la référence des professionnels de santé.
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