Estrogen increases inducible nitric oxide synthase gene expression

Walsh, Leigh S.; Ollendorff, Arthur; Mershon, John L.

doi:10.1067/mob.2003.350

Cited by 7 publications

(5 citation statements)

References 16 publications

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“… 12 , 14 In the present analysis of a relatively large population, male sex was independently and positively associated with elevated F eno levels, even after adjustment for smoking status and body size, which differed between men and women. The results of this study regarding sex differences are not consistent with the biological studies showing estrogen action on inducible nitric oxide synthase activity 23 , 24 , 25 and that an increase in androgen receptors is associated with a decrease in F eno . 26 Although the differences in their distribution indices, such as median, were small and unlikely to have a significant impact on actual clinical practice decisions, further investigation is needed to determine whether male sex is mechanistically associated with higher F eno .…”

Section: Discussioncontrasting

confidence: 99%

Fractional exhaled nitric oxide distribution and its relevant factors in the general adult population and its healthy subpopulation

Yamada,

Takase,

Nakaya

et al. 2024

Journal of Allergy and Clinical Immunology: Global

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Section: Discussioncontrasting

confidence: 99%

Fractional exhaled nitric oxide distribution and its relevant factors in the general adult population and its healthy subpopulation

Yamada,

Takase,

Nakaya

et al. 2024

Journal of Allergy and Clinical Immunology: Global

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“…The ex vivo and in vitro studies presented here identify a direct effect of estrogen on iNOS in macrophages, which was mediated through the estrogen receptor (our data and refs. [25,26]).…”

Section: Discussionmentioning

confidence: 99%

“…The production of NO, which is critical to Leishmania containment in the mouse model [21], is also enhanced by the high physiological levels of estrogen and progesterone in pregnant females of different species. In fact, NO is critical for controlling uterine contractility, cervical ripening, and feto-placental blood flow [22][23][24][25][26]. In pregnant rats, progesterone seems to act synergistically with NO, playing an important role in embryo implantation [27,28].…”

Section: Introductionmentioning

confidence: 99%

Pregnancy enhances the innate immune response in experimental cutaneous leishmaniasis through hormone-modulated nitric oxide production

Osorio

Bonilla

Peniche

et al. 2008

Journal of Leukocyte Biology

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The maintenance of host defense during pregnancy may depend on heightened innate immunity. We evaluated the immune response of pregnant hamsters during early infection with Leishmania (Viannia) panamensis, a cause of American cutaneous leishmaniasis. At 7 days post-infection, pregnant animals showed a lower parasite burden compared with nonpregnant controls at the cutaneous infection site (P=0.0098) and draining lymph node (P=0.02). Resident peritoneal macrophages and neutrophils from pregnant animals had enhanced Leishmania killing capacity compared with nonpregnant controls (P=0.018 each). This enhanced resistance during pregnancy was associated with increased expression of inducible NO synthase (iNOS) mRNA in lymph node cells (P=0.02) and higher NO production by neutrophils (P=0.0001). Macrophages from nonpregnant hamsters infected with L. panamensis released high amounts of NO upon estrogen exposure (P=0.05), and addition of the iNOS inhibitor L-N6-(1-iminoethyl) lysine blocked the induction of NO production (P=0.02). Infected, nonpregnant females treated with estrogen showed a higher percentage of cells producing NO at the infection site than controls (P=0.001), which correlated with lower parasite burdens (P=0.036). Cultured macrophages or neutrophils from estrogen-treated hamsters showed significantly increased NO production and Leishmania killing compared with untreated controls. iNOS was identified as the likely source of estrogen-induced NO in primed and naïve macrophages, as increased transcription was evident by real-time PCR. Thus, the innate defense against Leishmania infection is heightened during pregnancy, at least in part as a result of estrogen-mediated up-regulation of iNOS expression and NO production.

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“…Indeed, 17␤E has been shown to augment T cell responses as well as promote increases in the proinflammatory T helper 1 cytokine, interferon-␥ (27,69,121,123,164,194). 17␤E is also associated with increased expression of inducible NO synthase (253), which has been shown to mediate endothelial dysfunction in response to inflammatory stimuli such as LPS (88,89). Thus, 17␤E appears to have both antiand proinflammatory properties in the vasculature as well as in a number of distinct immune cell types.…”

Section: Effects Of 17␤e On the Inflammatory Response And Vascular Inflammationmentioning

confidence: 99%

Sex differences in the vascular function and related mechanisms: role of 17β-estradiol

Pabbidi

Kuppusamy

Didion

et al. 2018

American Journal of Physiology-Heart and Circulatory Physiology

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The incidence of cardiovascular disease (CVD) is lower in pre-menopausal women but increases with age and menopause compared to similar-aged men. Based on the prevalence of CVD in the post-menopausal women, sex hormone-dependent mechanisms have been postulated to be the primary factors responsible for the protection from CVD in pre-menopausal women. Recent Women's Health Initiative studies, Cochrane review, ELITE and KEEPS studies suggest that beneficial effects of hormone replacement therapy (HRT) are seen in women less than 60 years of age and if initiated in less than ten years of menopause. In contrast, the beneficial effects of HRT are not seen in women greater than 60 years of age and if commenced after ten years of menopause. The higher incidence of CVD and the failure of HRT in post-menopausal aged women could be partly associated with fundamental differences in the vascular structure and function between men and women and in between pre and post-menopausal women, respectively. In this regard, previous studies from human and animal studies identified several sex differences in the vascular function and the associated mechanisms. Female sex hormone 17βEstradiol (17βE) regulates the majority of these mechanisms. In this review, we summarize the sex differences in vascular structure, myogenic properties, endothelial-dependent and -independent mechanisms and the role of 17βE in the regulation of vascular function.

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Estrogen increases inducible nitric oxide synthase gene expression

Cited by 7 publications

References 16 publications

Fractional exhaled nitric oxide distribution and its relevant factors in the general adult population and its healthy subpopulation

Fractional exhaled nitric oxide distribution and its relevant factors in the general adult population and its healthy subpopulation

Pregnancy enhances the innate immune response in experimental cutaneous leishmaniasis through hormone-modulated nitric oxide production

Sex differences in the vascular function and related mechanisms: role of 17β-estradiol

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