Nitric oxide synthases and tubal ectopic pregnancies induced by Chlamydia infection: basic and clinical insights.

Molecular Human Reproduction
Ruijin ShaoHåkan Billig

Abstract

Human ectopic pregnancy (EP) remains a common cause of pregnancy-related first trimester death. Nitric oxide (NO) is synthesized from L-arginine by three NO synthases (NOS) in different tissues, including the Fallopian tube. Studies of knockout mouse models have improved our understanding of the function of NOS isoforms in reproduction, but their roles and specific mechanisms in infection-induced tubal dysfunction have not been fully elucidated. Here, we provide an overview of the expression, regulation and possible function of NOS isoforms in the Fallopian tube, highlighting the effects of infection-induced changes in the tubal cellular microenvironment (imbalance of NO production) on tubal dysfunction and the potential involvement of NOS isoforms in tubal EP after Chlamydia trachomatis genital infection. The non-equivalent regulation of tubal NOS isoforms during the menstrual cycle suggests that endogenous ovarian steroid hormones regulate NOS in an isoform-specific manner. The current literature suggests that infection with C. trachomatis induces an inflammatory response that eventually leads to tubal epithelial destruction and functional impairment, caused by a high NO output mediated by inducible NOS (iNOS). Therefore, tis...Continue Reading

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Citations

Feb 24, 2012·Biology of Reproduction·Ruijin ShaoHåkan Billig
Aug 7, 2012·The Australian & New Zealand Journal of Obstetrics & Gynaecology·Nicole StamatopoulosGeorge Condous
Jun 26, 2018·Reproduction, Fertility, and Development·Bredford KerrManuel Villalón
Sep 25, 2021·The Journal of Obstetrics and Gynaecology Research·Huan Jiang, Jian-Xiong Li

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Methods Mentioned

BETA
gene knockout
biopsies

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