Molecular mechanism of miR-181b in heart disease due to pregnancy-induced hypertension syndrome

Figures

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  Figure 1.. Expression of miR-181b in peripheral blood relative to U6 (fold). The expression of miR-181b was detected using reverse transcription-quantitative polymerase chain reaction. (A) Expression of miR-181b increased in the peripheral blood of patients with HDCP compared with normal control. (B) miR-181b expression decreased in patients in stage III and IV compared with stage II hypertension. (C) The expression of TIMP3 was significantly increased in peripheral blood samples of patients with HDCP. *P<0.05. miR, microRNA; HDCP, hypertensive disorder complicating pregnancy; TIMP3, metallopeptidase inhibitor 3.

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  Figure 2.. The correlation between miR-181b and TIMP3 expressions relative to controls at specific time points during culture in hypoxia. Assessed using reverse transcription-quantitative polymerase chain reaction. miR-181b expression was significantly decreased in a time-dependent manner in association with hypoxia. TIMP3 expression was significantly increased with the duration of hypoxia. *P<0.05 for miR-181b expression vs. 0 h, #P<0.05 for TIMP3 expression vs. 0 h. miR, microRNA; TIMP3, metallopeptidase inhibitor 3.

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  Figure 3.. Expression of TIMP3 in myocardial cells, detected by western blot analysis. (A) TIMP3 expression relative to U6 increased in myocardial cells following transfection with miR-181b inhibitor and decreased following transfection with miR-181b mimic, compared with the control group. (B) TIMP3 expression decreased in myocardial cells following transfection with siR-TIMP3 compared with control cells. *P<0.05 vs. NC. TIMP3, metallopeptidase inhibitor 3; miR, microRNA; NC, normal control; GAPDH, glyceraldehyde 3-phosphate dehydrogenase; siR-TIMP, TIMP3 short interfering RNA.

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  Figure 4.. miR-181b inhibits the apoptosis of myocardial cells. (A) Rate of apoptosis in myocardial cells following transfection with miR-181b was lower than that of the NC. (B) Rate of apoptosis in myocardial cells following transfection with siR-TIMP3 was lower than that of the NC. *P<0.05 vs. NC. miR, microRNA; NC, normal control; siR-TIMP3, metallopeptidase inhibitor 3 short interfering RNA; FITC, fluorescein isothiocyanate.

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  Figure 5.. TIMP3 is a direct target gene of miR-181b. (A) miR-181b seed sequence and binding sites on TIMP3 3′untranslated region (upper) and a number of base mutations. (B) Dual luciferase assay used to detect whether TIMP3 is regulated by miR-181b. Luciferase activity relative to controls. *P<0.05 vs. NC. TIMP3, metallopeptidase inhibitor 3; miR, microRNA; NC, normal control.