miR-19-3p Promotes Autophagy and Apoptosis in Pelvic Organ Prolapse Through the AKT/mTOR/p70S6K Pathway: Function of miR-19-3p on Vaginal Fibroblasts by Targeting IGF-1

被引:10
|
作者
Yin, Yitong [1 ]
Qin, Meiying [1 ]
Luan, Meng [1 ]
Xia, Zhijun [1 ]
机构
[1] China Med Univ, Shengjing Hosp, Dept Obstet & Gynecol, Pelv Floor Dis Diag & Treatment Ctr, Shenyang, Peoples R China
来源
FEMALE PELVIC MEDICINE AND RECONSTRUCTIVE SURGERY | 2021年 / 27卷 / 09期
关键词
miR-19-3p; IGF-1; pelvic organ prolapse; fibroblast; GROWTH-FACTOR-I; MESSENGER-RNA; FIBROSIS;
D O I
10.1097/SPV.0000000000001034
中图分类号
R71 [妇产科学];
学科分类号
100211 ;
摘要
Objective Pelvic organ prolapse (POP) is a common condition in older women. A decrease in collagen 1 (Col-1) expression is one of the main causes of POP. Many microRNAs play an important role in regulating target genes. The relationship between miR-19-3p and POP is investigated in this study, and the molecular mechanism was also explored to find whether miR-19-3p may be a potential target for early diagnosis and prevention of POP. Methods A total of 60 patients with POP and 60 patients without POP were included in this study. Reverse transcription-polymerase chain reaction and Western blot were used to detect the expression of miR-19-3p, insulin-like growth factor 1 (IGF-1), and the Akt/mTOR/p70S6K pathway. Cell cycle was defined by flow cytometric analysis. The combination of miR-19-3p and IGF-1 was revealed by luciferase assays. Results The results of this study show that miR-19-3p was upregulated in the tissue of patients with POP, whereas COL-1 and IGF-1 expressions were lower in the POP group. miR-19-3p promoted excessive fibroblast autophagy and apoptosis. miR-19-3p negatively regulated the Akt/mTOR/p70S6K pathway and inhibited COL-1 secretion. Luciferase reporter assay showed that miR-19-3p regulated IGF-1 expression by direct target binding. Conclusions miR-19-3p has negative associations with the expression of Col-1. Our study highlights that miR-19-3p may affect the synthesis of Col-1 by targeting IGF-1 and that it may play an vital role in POP.
引用
收藏
页码:E630 / E638
页数:9
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