Identification of nitric oxide synthase in human uterus

Telfer, Joan F.; Lyall, Fiona; Norman, Jane E.; Cameron, IT

doi:10.1093/humrep/10.1.19

Cited by 148 publications

(89 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The importance of NO as a regulator of early developmental events has been established by studies that demonstrated that the oocyte and preimplantation embryo are exposed to NO, and oocyte maturation, preimplantation embryogenesis and implantation require NO (Biswas et al, 1998;Gagioti et al, 2000;Maul et al, 2003;Novaro et al, 1997;Purcell et al, 1999;Sengoku et al, 2001;Shukovski and Tsafriri, 1995;Telfer et al, 1995). Moreover, in vitro and in vivo studies showed that administration of either NOS inhibitors or NO donors hinders development of preimplantation embryos (i.e.…”

Section: Introductionmentioning

confidence: 99%

Nitric oxide modulates murine yolk sac vasculogenesis and rescues glucose induced vasculopathy

et al. 2004

View full text Add to dashboard Cite

Nitric oxide (NO) has been demonstrated to mediate events during ovulation,pregnancy, blastocyst invasion and preimplantation embryogenesis. However,less is known about the role of NO during postimplantation development. Therefore, in this study, we explored the effects of NO during vascular development of the murine yolk sac, which begins shortly after implantation. Establishment of the vitelline circulation is crucial for normal embryonic growth and development. Moreover, functional inactivation of the endodermal layer of the yolk sac by environmental insults or genetic manipulations during this period leads to embryonic defects/lethality, as this structure is vital for transport, metabolism and induction of vascular development. In this study, we describe the temporally/spatially regulated distribution of nitric oxide synthase (NOS) isoforms during the three stages of yolk sac vascular development (blood island formation, primary capillary plexus formation and vessel maturation/remodeling) and found NOS expression patterns were diametrically opposed. To pharmacologically manipulate vascular development,an established in vitro system of whole murine embryo culture was employed. During blood island formation, the endoderm produced NO and inhibition of NO(L-NMMA) at this stage resulted in developmental arrest at the primary plexus stage and vasculopathy. Furthermore, administration of a NO donor did not cause abnormal vascular development; however, exogenous NO correlated with increased eNOS and decreased iNOS protein levels. Additionally, a known environmental insult (high glucose) that produces reactive oxygen species(ROS) and induces vasculopathy also altered eNOS/iNOS distribution and induced NO production during yolk sac vascular development. However, administration of a NO donor rescued the high glucose induced vasculopathy, restored the eNOS/iNOS distribution and decreased ROS production. These data suggest that NO acts as an endoderm-derived factor that modulates normal yolk sac vascular development, and decreased NO bioavailability and NO-mediated sequela may underlie high glucose induced vasculopathy.

show abstract

Section: Introductionmentioning

confidence: 99%

Nitric oxide modulates murine yolk sac vasculogenesis and rescues glucose induced vasculopathy

et al. 2004

View full text Add to dashboard Cite

show abstract

“…NOS activity has been reported to be present in the endometrium of nonpregnant sheep (24). Recently, Telfer et al (25) demonstrated the presence of eNOS mRNA and protein in human endometrium and myometrium using in situ hybridization and immunocytochemistry. Recent work has shown that human endometrial glandular cells express eNOS mRNA throughout the menstrual cycle, while the expression of iNOS mRNA is confined to epithelial glands isolated from menstrual endometrium (26).…”

Section: Discussionmentioning

confidence: 99%

Role of nitric oxide synthase in release of endothelin from cultured human endometrial cells

Kubota¹,

Masuda²,

Asô³

1998

European Journal of Endocrinology

View full text Add to dashboard Cite

The aim of this study was to investigate the influence of the nitric oxide/nitric oxide synthase (NO/NOS) system on the release of endothelin-1 (ET-1) in human endometrial cells. Human endometrial stromal cells in secretory phase were incubated for 72 h in serum-free RPMI 1640 medium in the absence or presence of different concentrations of interleukin-1b (IL-1b) and N G -monomethyl-L-arginine (LNMMA), a specific competitive inhibitor of NOS. ET-1 released from the cultured cells into the medium was determined by specific RIA. In all the experiments at various times, IL-1b significantly increased the release of ET-1. LNMMA significantly attenuated the release of ET-1 when the cells were cultured with both IL-1b and LNMMA, but LNMMA alone had no effect on ET-1 release. These results suggest that the NO/NOS system in human endometrium is involved in the regulation of ET-1 release via IL-1b secretion. It can also be inferred that NO and ET-1 control the functions of endometrium in close association with IL-1b.

show abstract

“…In mammals it is a potent vasodilator with short half-life, and an important cell signaling molecule that is involved in many physiological and pathological processes (Hou, 1999). It has been reported that localized NO synthesis in reproductive tissue plays an important role in regulating certain reproductive functions such as endometrial, cervical and myometrial activity (Telfer, 1995), embryo implantation (Battaglia, 2003) as well as embryo development (Chwalisz, 1999). While it is apparent from these studies that NO plays key roles in early pregnancy and even parturition, its concentration must be tightly regulated as it has also been reported that aberrant NO levels have been associated with embryo cytotoxicity (Barroso, 1999), early embryo loss (Haddad, 1995), as well as preterm labor (Cella, 2010).…”

Section: Introductionmentioning

confidence: 99%

The Progesterone Receptor – To Be or Not to Be: The Anti-Inflammatory Effects of Progesterone in RAW 264.7 Cells

George¹

2017

stem

View full text Add to dashboard Cite

It has been widely established that, in addition to its role in reproduction, progesterone (P4) also has potent anti-inflammatory effects. While the precise mechanisms have never been clearly elucidated in RAW 246.7 cells, it seems logical to assume that this response is -at least in part -a consequence of activation of and signaling through the progesterone receptor (P4-R). However, it has recently been shown that in a rat model, this anti-inflammatory effect is -in fact -independent of the progesterone receptor. In this project, the aim was to characterize this response by assaying nitric oxide production from lipopolysaccharide-challenged RAW 264.7 cells and ascertain the involvement of the P4-R. To determine the contribution of the receptor, RAW cells were incubated in the presence and absence of RU-486 -a potent P4-R antagonist. Our results indicate that the anti-inflammatory response of progesterone was in fact through the activation of the P4-R as cells incubated in RU-486 show an approximate 60% reversal of the inhibitory effect of P4 as compared to cells incubated in the absence of the antagonist. However, because we did not observe a complete reversal, suggests that perhaps other receptors come into play which will be addressed in future studies. Creative Commons LicenseThis work is licensed under a Creative Commons Attribution 4.0 License.This article is available in Proceedings of the Interdisciplinary STEM Teaching and Learning Conference:https://digitalcommons.georgiasouthern.edu/stem_proceedings/vol1/iss1/8 The Progesterone Receptor -To Be or Not to Be: The Anti-inflammatory Effects of Progesterone in RAW 264.7 CellsChristopher I Brandon Jr., Georgia Gwinnett College Bagie M. George, Georgia Gwinnett College Abstract: It has been widely established that, in addition to its role in reproduction, progesterone (P4) also has potent anti-inflammatory effects. While the precise mechanisms have never been clearly elucidated in RAW 246.7 cells, it seems logical to assume that this response is -at least in part -a consequence of activation of and signaling through the progesterone receptor (P4-R). However, it has recently been shown that in a rat model, this anti-inflammatory effect is -in fact -independent of the progesterone receptor. In this project, the aim was to characterize this response by assaying nitric oxide production from lipopolysaccharide-challenged RAW 264.7 cells and ascertain the involvement of the P4-R. To determine the contribution of the receptor, RAW cells were incubated in the presence and absence of RU-486 -a potent P4-R antagonist.Our results indicate that the anti-inflammatory response of progesterone was in fact through the activation of the P4-R as cells incubated in RU-486 show an approximate 60% reversal of the inhibitory effect of P4 as compared to cells incubated in the absence of the antagonist. However, because we did not observe a complete reversal, suggests that perhaps other receptors come into play which will be addressed in future studies.

show abstract

Identification of nitric oxide synthase in human uterus

Cited by 148 publications

References 0 publications

Nitric oxide modulates murine yolk sac vasculogenesis and rescues glucose induced vasculopathy

Nitric oxide modulates murine yolk sac vasculogenesis and rescues glucose induced vasculopathy

Role of nitric oxide synthase in release of endothelin from cultured human endometrial cells

The Progesterone Receptor – To Be or Not to Be: The Anti-Inflammatory Effects of Progesterone in RAW 264.7 Cells

Contact Info

Product

Resources

About