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Fig. 5 | Journal of Translational Medicine

Fig. 5

From: Atrial myocyte-derived exosomal microRNA contributes to atrial fibrosis in atrial fibrillation

Fig. 5

GPD1L is a target of miR-210-3p and may mediate its effects on fibrosis. A The site predicted GPD1L as a target gene. B RNA-Seq analysis of the differentially expressed mRNAs in the WT and miR-210-3p KO groups of rat hearts. Levels of the GPD1L (C) and Col11a2 (D) mRNAs were analyzed in atrial myocytes by qRT-PCR (*P < 0.05 and **P < 0.01). E The GPD1L protein expression level in the mimic and inhibitor groups of atrial myocytes (*P < 0.05 compared with the inhibitor NC; ***P < 0.001 compared with the mimic NC). F The GPD1L protein expression level in WT and KO groups of rats (n = 7; *P < 0.05). G The GPD1L protein expression level in atrial fibroblasts treated with atrial myocyte-derived exosomes in Ctr and EXO-Pacing groups (***P < 0.001). H Wild-type sequence (WT-GPD1L) and mutated sequence (MUT-GPD1L) for the miR-210-3p binding site. I Dual-luciferase expression is shown for GPD1L (***P < 0.001 compared with mimic NC)

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