MicroRNA-29a increased the intestinal membrane permeability of colonic epithelial cells in irritable bowel syndrome rats.

BACKGROUND: The whole pathogenesis of diarrhea-predominant irritable bowel syndrome(IBS-D) is poorly understood. Our goal was to evaluate the expression change of microRNA-29a(miR-29a) in colonic epithelial cells in IBS rats and clarify the mechanism of miR-29a increasing the intestinal membrane permeability through aquaporins(AQPs). METHODS: The IBS-D rats models were induced by rectal distention pressure combining with extremities constraint. The colonic epithelial cells were divided into four groups. A: normal group. B: IBS-D control group. C: IBS-D +miR-29a NC. D: IBS-D + miR-29a antagomir. The expression of miR-29a, the concentration of the K(+) and Lactate Dehydrogenase(LDH) and the expression of AQPs were detected. RESULTS: The miR-29a expression increased in IBS-D control group(2.090±0.022) compared with the control group(1.00±0.031) (P<0.001) while it decreased in IBS-D+miR-29a antagomir group(1.403±0.042) compared with IBS-D control group(P<0.001). The K(+) decreased in IBS-D control group(1.305±0.289) compared with the control group(2.171±0.204)(P<0.05) while it increased in IBS-D+miR-29a antagomir group(1.813±0.102)(P<0.05) compared with IBS-D control group. The LDH increased in IBS-D control group(4153.440±177.365) compared with the control group(1434.573±96.111)(P<0.001) while it decreased in IBS-D+miR-29a antagomir group(2700.473±275.414) compared with IBS-D control group (P<0.01). The expression of AQP1, AQP3 and AQP8 decreased in IBS-D control group(0.132±0.010,0.110±0.005,0.108±0.007) compared with the control group (P<0.001) while it increased in IBS-D+miR-29a antagomir group(0.197±0.005,0.182±0.011,0.194±0.003) compared with IBS-D control group(P<0.001). The IBS-D+miR-29a negative control(NC) group, a comparison with IBS-D+miR-29a antagomir group, each date showed the similar trend to the IBS-D control group. CONCLUSIONS: MiR-29a increased the intestinal membrane permeability of colonic epithelial cells by reducing the AQPs expression in IBS-D rats.