Estradiol receptors agonists induced effects in rat intestinal microcirculation during sepsis

Sharawy, Nivin; Ribback, Silvia; Al-Banna, Nadia; Lehmann, Christian; Kern, Hartmut; Wendt, Michael; Černý, V.; Dombrowski, Frank; Pavlović, Dragan

doi:10.1016/j.mvr.2012.10.002

Cited by 25 publications

(17 citation statements)

References 57 publications

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“…Female animals and women appear less prone to develop sepsis than males [68, 94, 106, 110]. Among the factors implicated in this difference are estrogen and its interactions with EC and WBC [83], estrogen receptor distribution [106], sex differences in glucocorticoid action [17], and inflammatory status [9], to name but a few identified factors.…”

Section: Venulesmentioning

confidence: 99%

Sex-Specific Characteristics of the Microcirculation

Huxley

Kemp

2018

Advances in Experimental Medicine and Biology

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The requirements of metabolizing tissue are both continuous and variable; accordingly, the microvasculature serving that tissue must be similarly dynamic. Just as it is recognized that males and females of the same species have differing metabolic requirements, is it not likely that the microvasculature serving these tissues will differ by sex? This section focusing on the constituents of the microcirculation identifies what is known presently about the role sex plays in matching metabolic demand with microvascular function and areas requiring additional study. Many of the identified sex differences are subtle and easily ignored. In the aggregate, though, they can profoundly alter phenotype, especially under stressful conditions including pregnancy, exercise, and disease states ranging from diabetes to heart failure. Although the features presently identified to “have sex” range from differences in growth, morphology, protein expression, and intracellular signaling, males and females alike achieve homeostasis, likely by different means. Studies of microvascular sexual dimorphism are also identifying age as an independent but interacting factor requiring additional attention. Overall, attempting to ignore either sex and/or age is inappropriate and will prevent the design and implementation of appropriate interventions to present, ameliorate, or correct microvascular dysfunction.

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Section: Venulesmentioning

confidence: 99%

Sex-Specific Characteristics of the Microcirculation

Huxley

Kemp

2018

Advances in Experimental Medicine and Biology

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“…In this respect, several studies involving males and ovariectomized females given exogenous estrogen indicated that females might be better positioned in mitigating against pathology from microcirculatory disorder and sepsis 48 , 49 . In particular, Sharawy et al showed that independent of whether septic males or ovariectomized females were treated with agonists for the estrogen receptor (ER)-α or -β, a significantly reduced sepsis-induced leukocyte–endothelial interaction (rolling, adherent leukocytes and neutrophil extravasations) and improved intestinal muscular functional capillary density was observed 56 . Those results suggest that the observed effects of estradiol receptors on different phases of leukocyte recruitment with the improvement of the functional capillary density could partially explain salutary effects of estradiol on the intestinal microcirculation during sepsis.…”

Section: Sex Steroids Differently Affect the Cardiovascular Systemmentioning

confidence: 99%

Gender differences in sepsis

Angele¹,

Pratschke²,

et al. 2013

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During sepsis, a complex network of cytokine, immune, and endothelial cell interactions occur and disturbances in the microcirculation cause organ dysfunction or even failure leading to high mortality in those patients. In this respect, numerous experimental and clinical studies indicate sex-specific differences in infectious diseases and sepsis. Female gender has been demonstrated to be protective under such conditions, whereas male gender may be deleterious due to a diminished cell-mediated immune response and cardiovascular functions. Male sex hormones, i.e., androgens, have been shown to be suppressive on cell-mediated immune responses. In contrast, female sex hormones exhibit protective effects which may contribute to the natural advantages of females under septic conditions. Thus, the hormonal status has to be considered when treating septic patients. Therefore, potential therapies could be derived from this knowledge. In this respect, administration of female sex hormones (estrogens and their precursors) may exert beneficial effects. Alternatively, blockade of male sex hormone receptors could result in maintained immune responses under adverse circulatory conditions. Finally, administration of agents that influence enzymes synthesizing female sex hormones which attenuate the levels of pro-inflammatory agents might exert salutary effects in septic patients. Prospective patient studies are required for transferring those important experimental findings into the clinical arena.

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“…Other studies have observed that ERα-specific agonists influence leukocyte rolling and adhesion to protect against sepsis in the colon, demonstrating that ERα has a protective roll in the tissue [21]. GPER has also been implicated in mitigating inflammation; treatment of endothelial cells with a GPER-specific agonist has been demonstrated to reduce the expression of pro-inflammatory cytokines [22].…”

Section: Discussionmentioning

confidence: 99%

Estradiol Has Differential Effects on Acute Colonic Inflammation in the Presence and Absence of Estrogen Receptor β Expression

et al. 2017

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Background Inflammatory bowel disease (IBD) increases the risk of developing colon cancer. This risk is higher in men compared to women, implicating a role for female hormones in the protection against this disease. Studies from our laboratory demonstrated that estradiol (E2) protects against inflammation-associated colon tumor formation when administered following chemical carcinogen and induction of chronic colitis. Aim This study seeks to better understand the effect of E2 on acute colitis in the presence and absence of estrogen receptor β (ERβ). Methods Inflammation was induced by 2,4,6-trinitrobenzenesulfonic acid in wild-type (WT) and ERβ knockout (ERβKO) mice implanted with a control or E2-containing pellet and killed 5 days later. Inflammation and injury were scored by a pathologist. Apoptosis and proliferation were assessed by immunohistochemistry. Cytokines were measured by multiplex analysis. Results E2 treatment reduced inflammation in the middle colon in WT mice and the distal colon in ERβKO mice compared to control mice. WT mice had reduced IL-6, IL-12, IL-17, GM-CSF, IFN-γ, MCP-1, MIP-1α, and TNF-α, and ERβKO had reduced IL-6 and IFN-γ expression in response to E2. Injury scores were lower in E2-treated ERβKO mice compared to control ERβKO mice. ERβKO mice had increased proliferation in the basal third of crypts in the distal colon and decreased apoptosis in the proximal colon. Conclusions These data suggest that E2 has differential protective effects against acute colitis in the presence or absence of ERβ and provide insight into how E2 may protect against IBD.

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Estradiol receptors agonists induced effects in rat intestinal microcirculation during sepsis

Cited by 25 publications

References 57 publications

Sex-Specific Characteristics of the Microcirculation

Sex-Specific Characteristics of the Microcirculation

Gender differences in sepsis

Estradiol Has Differential Effects on Acute Colonic Inflammation in the Presence and Absence of Estrogen Receptor β Expression

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