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The regulation of nitric oxide synthase isoform expression in mouse and human fallopian tubes: Potential insights for ectopic pregnancy

Journal article
Authors Junting Hu
S. Ma
S. Zou
X. Li
P. Cui
Birgitta Weijdegård
G. Wu
Linus Ruijin Shao
Håkan Billig
Yi Feng
Published in International Journal of Molecular Sciences
Volume 16
Issue 1
Pages 49-67
ISSN 1422-0067
Publisher MDPI AG
Publication year 2015
Published at Institute of Neuroscience and Physiology, Department of Physiology
Pages 49-67
Language en
Keywords Ectopic pregnancy, Fallopian tube, Nitric oxide synthase, Steroid hormones, endothelial nitric oxide synthase, estradiol, inducible nitric oxide synthase, lactate dehydrogenase, luteinizing hormone, messenger RNA, neuronal nitric oxide synthase, progesterone, adult, animal experiment, animal tissue, Article, controlled study, enzyme activity, female, human, human tissue, immunofluorescence, immunohistochemistry, menstrual cycle, mouse, muscle contractility, nonhuman, ovulation, protein expression, real time polymerase chain reaction, regulatory mechanism, reverse transcription polymerase chain reaction, RNA extraction, uterine tube, Mus
Subject categories Physiology, Obstetrics and gynaecology


Nitric oxide (NO) is highly unstable and has a half-life of seconds in buffer solutions. It is synthesized by NO-synthase (NOS), which has been found to exist in the following three isoforms: neuro nitric oxide synthase (nNOS), inducible nitric oxide synthase (iNOS), and endothelial nitric oxide synthase (eNOS). NOS activity is localized in the reproductive tracts of many species, although direct evidence for NOS isoforms in the Fallopian tubes of mice is still lacking. In the present study, we investigated the expression and regulation of NOS isoforms in the mouse and human Fallopian tubes during the estrous and menstrual cycles, respectively. We also measured isoform expression in humans with ectopic pregnancy and in mice treated with lipopolysaccharide (LPS). Our results confirmed the presence of different NOS isoforms in the mouse and human Fallopian tubes during different stages of the estrous and menstrual cycles and showed that iNOS expression increased in the Fallopian tubes of women with ectopic pregnancy and in LPS-treated mice. Elevated iNOS activity might influence ovulation, cilia beats, contractility, and embryo transportation in such a manner as to increase the risk of ectopic pregnancy. This study has provided morphological and molecular evidence that NOS isoforms are present and active in the human and mouse Fallopian tubes and suggests that iNOS might play an important role in both the reproductive cycle and infection-induced ectopic pregnancies.

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