TY - JOUR
T1 - Nitric oxide synthases and tubal ectopic pregnancies induced by Chlamydia infection
T2 - Basic and clinical insights
AU - Shao, Ruijin
AU - Zhang, Sean X.
AU - Weijdegård, Birgitta
AU - Zou, Shien
AU - Egecioglu, Emil
AU - Norström, Anders
AU - Brännström, Mats
AU - Billig, Håkan
N1 - Funding Information:
This review was supported by the Swedish Medical Research Council (Grant 5859), the Sahlgrenska Academy Research Council, the Mary von Sydow Foundation and Göteborgs Läkaresällskap. Funding to pay the Open Access Charge was provided by the Swedish Research Council.
PY - 2010/12
Y1 - 2010/12
N2 - 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, tissue-specific therapeutic approaches to suppress iNOS expression may help to prevent ectopic implantation in patients with prior C. trachomatis infection of the Fallopian tube.
AB - 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, tissue-specific therapeutic approaches to suppress iNOS expression may help to prevent ectopic implantation in patients with prior C. trachomatis infection of the Fallopian tube.
KW - Chlamydia trachomatis
KW - Nitric oxide
KW - Nitric oxide synthase isoforms
KW - Tubal ectopic pregnancy
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U2 - 10.1093/molehr/gaq063
DO - 10.1093/molehr/gaq063
M3 - Review article
C2 - 20647263
AN - SCOPUS:78249234056
SN - 1360-9947
VL - 16
SP - 907
EP - 915
JO - Molecular Human Reproduction
JF - Molecular Human Reproduction
IS - 12
M1 - gaq063
ER -