Abstract

Objective To establish a mouse model of neurogenic bladder and to investigate the changes of fibronectin 1 (FN1) and the action mechanism of microRNA (miRNA, miR)-1a-3p. Methods Mice were divided into model group and control group. The model group received subcutaneous injection of myelin oligodendrocyte glycoprotein and mycobacterium tuberculosis, and intraperitoneal injection of pertussis toxin at 48 h. The control group received subcutaneous injection of normal saline. The frequency of urination and the amount of urine output were observed. The mice were sacrificed and the bladder tissue was taken. Three bladders were selected from the model group and the control group for high-throughput sequencing. The changes of FN1 and miR-1a-3p in mouse bladder tissues were detected by real-time quantitative reverse transcription polymerase chain reaction (RT-qPCR) and Western blotting. Results The sequencing results were analyzed. As the urinary system symptoms worsened, FN1 increased (4.569±0.426, t=-5.142, P<0.01), while miR-1a-3p decreased (1.623±0.312, t=-3.945, P<0.05). Compared with the control group, the expression of FN1 mRNA [2.501 (1.301, 4.251), F=99.183, P<0.01] and protein [2.937 (1.174, 4.262), F=63.834, P<0.01] in the bladder tissue of the model group was up-regulated, and that of miR-1a-3p was down-regulated [2.401 (1.250, 3.001), F=35.951, P<0.01]. The dual luciferase gene report indicated that FN1 was a direct target gene of miR-1a-3p (0.514±0.027, t=13.355, P<0.01). Conclusion The animal model of neurogenic bladder has urinary frequency, urgency, urinary retention and other symptoms, and the expression of FN1 is up-regulated, while the expression of miR-1a-3p is down-regulated. Therefore, miR-1a-3p may participate in neurogenic bladder formation through regulation of FN1. Key words: Neurogenic bladder; Fibronectin 1; MicroRNA-1a-3p

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