Nitric oxide synthase inhibition and the uterotrophic response to oestrogen in immature rats

Rao, Venkata; Chaves, M. C.; Ribeiro, Rosângela Almeida

doi:10.1530/jrf.0.1050303

Cited by 13 publications

(5 citation statements)

References 1 publication

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…Although not represented on the microarray, Nos3 was found by QRT-PCR to be induced twofold at 2-8 h (data not shown). Inhibitors of nitric oxide synthase block estrogen-induced uterine edema and growth that can be overcome by pretreatment with exogenous arginine (56). Consequently, these activated pathways converge to promote uterine growth and remodeling.…”

Section: A Proposed Model For Arginine and Ornithine Utilizationmentioning

confidence: 99%

Identification of temporal patterns of gene expression in the uteri of immature, ovariectomized mice following exposure to ethynylestradiol

Fertuck

Eckel

Gennings

et al. 2003

Physiological Genomics

View full text Add to dashboard Cite

Estrogen induction of uterine wet weight provides an excellent model to investigate relationships between changes in global gene expression and well-characterized physiological responses. In this study, time course microarray GeneChip data were analyzed using a novel approach to identify temporal changes in uterine gene expression following treatment of immature ovariectomized C57BL/6 mice with 0.1 mg/kg 17alpha-ethynylestradiol. Functional gene annotation information from public databases facilitated the association of changes in gene expression with physiological outcomes, which allowed detailed mechanistic inferences to be drawn regarding cell cycle control and proliferation, transcription and translation, structural tissue remodeling, and immunologic responses. These systematic approaches confirm previously established responses, identify novel estrogen-regulated transcriptional effects, and disclose the coordinated activation of multiple modes of action that support the uterotrophic response elicited by estrogen. In particular, it was possible to elucidate the physiological significance of the dramatic induction of arginase, a classic estrogenic response, by elucidating its mechanistic relevance and delineating the role of arginine and ornithine utilization in the estrogen-stimulated induction of uterine wet weight.

show abstract

Section: A Proposed Model For Arginine and Ornithine Utilizationmentioning

confidence: 99%

Identification of temporal patterns of gene expression in the uteri of immature, ovariectomized mice following exposure to ethynylestradiol

Fertuck

Eckel

Gennings

et al. 2003

Physiological Genomics

View full text Add to dashboard Cite

show abstract

“…The vasoregulatory role of NO is well documented [11]. It has been hypothesized that NO is involved as an effector molecule in mediation of the effect of oestrogen on the uterus [12]. Progesterone also appears to influence uterine NO production because antiprogestins have been reported to reduce the NOS II isozyme, the major isoform of NOS that is responsible for upregulation of NO production during pregnancy [13].…”

Section: Introductionmentioning

confidence: 99%

Potential role of intermedin/adrenomedullin 2 in early embryonic development in rats

Chauhan

Elkins

Balakrishnan

et al. 2011

Regulatory Peptides

View full text Add to dashboard Cite

Adrenomedullin2 (ADM2), also referred to as Intermedin (IMD) is expressed in trophoblast cells in human placenta and enhances the invasion and migration of first trimester HTR-8/SV-neo cells. Recently we demonstrated that infusion of IMD antagonist in pregnant rats causes feto-placental growth restriction suggesting a role for IMD in maintaining a successful pregnancy. Therefore, this study was undertaken to assess if IMD has a functional role in embryo implantation in a rat model. We show that IMD mRNA is expressed in rat implantation sites and its expression is significantly higher on day 15 in placenta compared to days 18 – 22. Infusion of IMD antagonist IMD17–47 from day 3 of pregnancy causes a significant decrease in the weights of day 9 implantation sites as well as serum levels of 17β-estradiol, progesterone, nitric oxide and serum MMP2 and MMP9 gelatinase activity. Further, expression of MMP2,MMP9, VEGF and PLGF protein levels are significantly downregulated in the implantation sites of IMD antagonist treated rats. This study suggests a potential involvement of IMD in regulating the factors that are critical for implantation and growth of the embryo and thus in establishment of normal rat pregnancy.

show abstract

“…In connection with this association, oestrogen, more so than progesterone, regulated NOS isoforms and NO generation in the rat uterus 5 . Furthermore, N G ‐nitro‐ L ‐arginine methyl ester, an inhibitor of NOS, prevented oestradiol‐induced increases in uterine growth in immature rats 46 . Other relevant studies on dexamethasone and ovarian steroid interaction have noted that dexamethasone negatively affects oestrogen levels during embryonic development in pregnant rats 47 and is able to impair oestradiol‐induced uterine growth 48 .…”

Section: Discussionmentioning

confidence: 93%

Dexamethasone‐induced Changes in Endometrial Growth and Inducible Nitric Oxide Synthase During Decidualization in Rats

Spencer

Chi²,

Zhu³

1998

Clin Exp Pharma Physio

View full text Add to dashboard Cite

1. The present study investigated the time-dependent inhibitory responses of endometrial growth and inducible nitric oxide synthase (iNOS) to dexamethasone during deciduoma development that was surgically induced on day 4 of pseudopregnancy (PG). 2. Groups of rats (n = 6) were subcutaneously injected with dexamethasone (1.5 mg/rat per day) for 3 days (PG days 1-3, 4-6, 7-9, 10-12 and 12-15). Rats in each group were killed on the last injection day. 3. Dexamethasone produced comparable temporal inhibitory changes in endometrial growth (wet weight, protein and DNA concentrations; P<0.0001) and in iNOS activity (130 kDa protein band), which peaked after PG days 4-6 and 7-9 pretreatments. 4. Endometrial matrix metalloproteinases (72 and 92 kDa) activity profiles displayed maximal reductions (36 and 53%, respectively) following PG days 4-6 pretreatment. Serum progesterone levels were equally (P<0.0001) but asynchronously inhibited by dexamethasone on PG days 9 and 12. 5. Dexamethasone inhibition of endometrial growth and in situ iNOS was most pronounced during decidual development (PG days 4-9). Minor reductions in these endometrial parameters occurred before deciduoma induction (PG days 1-3) and during deciduoma regression (PG days 10-15). 6. These results indicate that, in the endometrium, the iNOS/endogenous nitric oxide system may be linked to the biochemical and metabolic mechanisms responsible for the developmental responsiveness of the deciduoma to dexamethasone exposure. These time-dependent changes in endometrial growth and iNOS apparently were not mediated by progesterone.

show abstract

Nitric oxide synthase inhibition and the uterotrophic response to oestrogen in immature rats

Cited by 13 publications

References 1 publication

Identification of temporal patterns of gene expression in the uteri of immature, ovariectomized mice following exposure to ethynylestradiol

Identification of temporal patterns of gene expression in the uteri of immature, ovariectomized mice following exposure to ethynylestradiol

Potential role of intermedin/adrenomedullin 2 in early embryonic development in rats

Dexamethasone‐induced Changes in Endometrial Growth and Inducible Nitric Oxide Synthase During Decidualization in Rats

Contact Info

Product

Resources

About