Overexpression of miR-27b-3p Targeting Wnt3a Regulates the Signaling Pathway of Wnt/β-Catenin and Attenuates Atrial Fibrosis in Rats with Atrial Fibrillation

Figures

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  Figure 1. miR-27b-3p negatively regulated the expression of Wnt3a (n = 6 for each group). (a) and (b) predicted binding sequence of miR-27b-3p and Wnt3a in rat and human. (c) Quantitative analysis of luciferase reporter gene results by Prism 6.0 software. Note that aP < 0.05 against the miR-27b-3p+MT group.

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  Figure 2. miR-27b-3p overexpression could reduce the incidence and duration of AF (n = 8 for each group). (a) Successful establishment of the AF rat model. (b) Incidence of AF. (c) Duration of AF. (d) The level of miR-27b-3. Note that aP < 0.05 against the sham group; bP < 0.05 against the AF group; cP < 0.05 against the AF group.

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  Figure 3. miR-27b-3p overexpression did not have a significant effect on the cardiac function (n = 8 for each group). (a) EF: left ventricular ejection fraction. (b) FS: left ventricular fractional shortening. (c) LVESD: left ventricular end-systolic diameter. (d) LVEDd: left ventricular end-diastolic diameter.

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  Figure 4. miR-27b-3p overexpression did not have a significant effect on myocardial enzyme (n = 8 for each group). (a) Serum level of cTnT. (b) Serum level of CK-MB.

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  Figure 5. Effects of miR-27b-3p overexpression on atrial fibrosis (n = 8 for each group). (a) Representative images of Masson's trichrome staining (×400) in the left atrial tissues of each group. (b) The degree of myocardial fibrosis was analyzed by the Image-Pro 6.0 software. Note that aP < 0.05 against the sham group; bP < 0.05 against the AF group; cP < 0.05 against the AF group.

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  Figure 6. Effects of miR-27b-3p overexpression on atrial fibrosis (n = 8 for each group). (a) Representative images of immunohistochemistry staining (×400) in the left atrial tissues of each group. (b, c) The quantitative analyses by the Image-Pro 6.0 software. Note that aP < 0.05 against the sham group; bP < 0.05 against the AF group; cP < 0.05 against the AF group.

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  Figure 7. Effects of miR-27b-3p overexpression on atrial fibrosis (n = 8 for each group). (a) Expression level of markers of fibrosis in the myocardial tissues detected using western blot and quantitative analyses by the Image-Pro 6.0 software (b–e). Note that aP < 0.05 against the sham group; bP < 0.05 against the AF group; cP < 0.05 against the AF group.

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  Figure 8. miR-27b-3p overexpression increased the expression of atrial CX43 (n = 8 for each group). (a) Representative images from the immunofluorescence staining (×400) in left atrial tissues. Red fluorescence represents CX43; blue fluorescence represents nuclei of total cardiac myocytes. (b) The quantitative analyses by the Image-Pro 6.0 software. (c) Expression of CX43 in the atrial tissues detected using western blot and quantitative analyses by the Image-Pro 6.0 software (d). Note that aP < 0.05 against the sham group; bP < 0.05 against the AF group; cP < 0.05 against the AF group.

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  Figure 9. miR-27b-3p overexpression attenuated the expression of the Wnt/β-Catenin signaling pathway (n = 8 for each group). (a) The level of Wnt3a. (b) Expression of Wnt3a and p-β-Catenin in the atrial tissues detected using western blot and quantitative analyses by the Image-Pro 6.0 software (c, d). Note that aP < 0.05 against the sham group; bP < 0.05 against the AF group; cP < 0.05 against the AF group.

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  Figure 10. The molecular mechanism diagram showed that miR-27b-3p played an important role in atrial fibrosis and the occurrence of AF by regulation of the signaling pathway of Wnt/β-Catenin through targeted Wnt3a.