Mitofusin2 regulates the proliferation and function of fibroblasts: possible mechanisms of pelvic organ prolapse
IUGA Academy. Lu Y. Jun 30, 2018; 212844; 488 Topic: Pelvic Organ Prolapse

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Mitofusin2 regulates the proliferation and function of fibroblasts: Possible mechanisms of pelvic organ prolapse

Wang, X1; Wang, X1; Zhou, Y1; Peng, C1; Chen, H2;Lu, Y1

1: Department of Obstetrics & Gynecology, Peking University First Hospital; 2: Department of Obstetrics and Gynecology, Beijing Tsinghua Changgeng Hospital

Introduction: A limited number of studies have focused on the relationship between pelvic organ prolapse (POP) and Mitofusin2(Mfn2), both of which are associated with aging.

Objective: The present study aimed to investigate the effects of Mfn2 on the proliferation of human uterosacral ligament fibroblasts and on the expression of procollagen as well as to identify the possible signal transduction pathway that is involved in the development of POP.

Methods: Uterosacral ligaments were harvested from POP and Non-Pelvic Organ Prolapse(NPOP) patients for fibroblast culture and characterization. Cellular activity and cell cycle were assessed following transfection by overexpressing and inhibitory Mfn2 Lentiviral Vectors. The expression levels of Mfn2, procollagen 1A1/1A2/3A1, P21waf1, cyclin dependent kinase 2(CDK-2), Raf-1, extracellular signal-regulated kinase 1/2 (ERK1/2) proteins and phosphorylation levels of Raf-1 and ERK1/2 were examined by Western-Blot.

Results: The overexpression of Mfn2 resulted in the increased proliferation and G0/G1 phase arrest of the majority of the cells. Concomitantly, the relative expression levels of procollagen 1A1/1A2/3A1, CDK2 and the phosphorylation levels of ERK1/2 and Raf-1 proteins were significantly decreased, while the levels of the P21waf1 protein were increased in the Mfn2 overexpressing group. The opposite results were noted for the RNAi group.

Conclusions: The cell cycle of the fibroblasts, cellular proliferation and levels of the procollagen proteins could be inhibited by the Ras-Raf-ERK axis as a result of the increase of Mfn2 during the development of POP. The data add insight into the pathogenesis, clinical prediction, individual diagnosis and treatment of POP.


Work supported by industry: no.

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