Protective Effect of Estradiol on Acute Lung Inflammation Induced by an Intestinal Ischemic Insult is Dependent on Nitric Oxide

Breithaupt‐Faloppa, Ana Cristina; Fantozzi, Evelyn Thaís; Assis-Ramos, M.M.; Vitoretti, Luana Beatriz; Couto, Gisele Kruger; Rossoni, Luciana Venturini; Oliveira‐Filho, Ricardo Martins; Vargäftig, B. Boris; Tavares-de-Lima, Wothan

doi:10.1097/shk.0b013e3182a01e24

Cited by 47 publications

(43 citation statements)

References 31 publications

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“…MiRNA-126, -34a, -155, and -125b expression in serum exosomes were determined by realtime PCR. Lung permeability was determined using Evans blue dye as previous described (30 EPCs in peripheral blood were determined as described (10). Cells were stained with the following antibodies: FITC-antimouse-CD34 antibody (eBioscience, San Diego, CA) and PE-antimouse-FLK-1 (BD Biosciences, San Diego, CA).…”

Section: Clpmentioning

confidence: 99%

Endothelial Progenitor Cells and a Stromal Cell–derived Factor-1α Analogue Synergistically Improve Survival in Sepsis

Goodwin

Chang²,

Zingarelli

et al. 2014

Am J Respir Crit Care Med

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Rationale: Endothelial progenitor cells (EPCs) have been associated with human sepsis but their role is incompletely understood. Stromal cell-derived factor (SDF)-1a facilitates EPC recruitment and is elevated in murine sepsis models. Previous studies have demonstrated that the SDF-1a analog CTCE-0214 (CTCE) is beneficial in polymicrobial sepsis induced by cecal ligation and puncture (CLP) in mice.Objectives: We hypothesized that exogenously administered EPCs are also beneficial in CLP sepsis and that CTCE provides synergistic benefit.Methods: Mice were subjected to CLP and administered EPCs at varying doses, CTCE, or a combination of the two. Mouse survival, plasma miRNA expression, IL-10 production, and lung vascular leakage were determined. The in vitro effect of CTCE on miRNA expression and EPC function were determined.Measurements and Main Results: Survival was improved with EPC therapy at a threshold of 10 6 cells. In coculture studies, EPCs augmented LPS-induced macrophage IL-10 production. In vivo EPC administration in sepsis increased plasma IL-10, suppressed lung vascular leakage, attenuated liver and kidney injury, and augmented miR-126 and -125b expression, which regulate endothelial cell function and/or inflammation. When subthreshold numbers of EPCs were coadministered with CTCE in CLP mice they synergistically improved survival. We demonstrated that CTCE recruits endogenous EPCs in septic mice. In in vitro analysis, CTCE enhanced EPC proliferation, angiogenesis, and prosurvival signaling while inhibiting EPC senescence. These cellular effects were, in part, explained by the effect of CTCE on miR-126, -125b, -34a, and -155 expression in EPCs.Conclusions: EPCs and CTCE represent important potential therapeutic strategies in sepsis.

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Section: Clpmentioning

confidence: 99%

Endothelial Progenitor Cells and a Stromal Cell–derived Factor-1α Analogue Synergistically Improve Survival in Sepsis

Goodwin

Chang²,

Zingarelli

et al. 2014

Am J Respir Crit Care Med

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“…Averring the findings of this study, it is also suggested that female-to-male transplantation is worse than male-to-male one 8,9,11 , which is probably due to the absence of protective effect of female hormones found at male subjects, but not at female ones 13,16 .…”

mentioning

confidence: 83%

“…In addition, gender-related hormonal differences may play a role in the acute lung lesion due to intestinal ischemia/reperfusion injury 13 .…”

Section: Plasmatic Hormonal Levelsmentioning

confidence: 99%

“…Female sex hormones play an important role in the preservation of functionality of various organs and systems. As female rats present a better response to shock, trauma and sepsis when compared to male rats, several studies state that female hormones (estradiol, mainly) have a protective action modulating the generation of inflammatory mediators [13][14][15] . It has been shown that estrogen is also a protective factor to infections, reason why women would be more resistant than men 14 .…”

Section: Introductionmentioning

confidence: 99%

“…The present study demonstrated that female subjects do not tolerate well the acute absence of estradiol. Its lack is known to be a deleterious factor to female organs 12 , and that is why female rats present damages more relevant than the other groups of animals since this hormone has an important role as a modulator of the immune response 13,16 . Hormonal replacement is already included in some protocols of brain dead organs transplantation 28 .…”

mentioning

confidence: 99%

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Sex differences on solid organ histological characteristics after brain death1

Simão

Ferreira²,

Kudo³

et al. 2016

Acta Cir. Bras.

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Brazil. CNPq Researcher, level 1D. Scientific and intellectual content of the study; conception and design of the study; analysis and interpretation of data; statistical analysis; manuscript preparation and writing; critical revision; final approval. ABSTRACT PURPOSE:To investigate gender differences in the evolution of the inflammatory process in rats subjected to brain death (BD). METHODS:Adult Wistar rats were divided into three groups: female; ovariectomized female; and male rats. BD was induced using intracranial balloon inflation and confirmed by maximal pupil dilatation, apnea, absence of reflex, and drop of mean arterial pressure. Six hours after BD, histological evaluation was performed in lungs, heart, liver and kidneys, and levels of inflammatory proteins, estrogen, progesterone, and corticosterone were determined in plasma. RESULTS:In the lungs, females presented more leukocyte infiltration compared to males (p<0.01). Ovariectomized female rat lungs were more hemorrhagic compared to other groups (p<0.001). In the heart, females had higher leukocyte infiltration and tissue edema compared to males (p<0.05). In the liver and kidneys, there were no differences among groups. In female group estradiol and progesterone were sharply reduced 6 hours after BD (p<0.001) to values observed in ovariectomized females and males. Corticosterone levels were similar. CONCLUSIONS:Sex hormones influence the development of inflammation and the status of organs. The increased inflammation in lungs and heart of female rats might be associated with the acute reduction in female hormones triggered by BD.

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Hemorrhagic Shock and the Microvasculature

Filho

2017

Comprehensive Physiology

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The microvasculature plays a central role in the pathophysiology of hemorrhagic shock and is also involved in arguably all therapeutic attempts to reverse or minimize the adverse consequences of shock. Microvascular studies specific to hemorrhagic shock were reviewed and broadly grouped depending on whether data were obtained on animal or human subjects. Dedicated sections were assigned to microcirculatory changes in specific organs, and major categories of pathophysiological alterations and mechanisms such as oxygen distribution, ischemia, inflammation, glycocalyx changes, vasomotion, endothelial dysfunction, and coagulopathy as well as biomarkers and some therapeutic strategies. Innovative experimental methods were also reviewed for quantitative microcirculatory assessment as it pertains to changes during hemorrhagic shock. The text and figures include representative quantitative microvascular data obtained in various organs and tissues such as skin, muscle, lung, liver, brain, heart, kidney, pancreas, intestines, and mesentery from various species including mice, rats, hamsters, sheep, swine, bats, and humans. Based on reviewed findings, a new integrative conceptual model is presented that includes about 100 systemic and local factors linked to microvessels in hemorrhagic shock. The combination of systemic measures with the understanding of these processes at the microvascular level is fundamental to further develop targeted and personalized interventions that will reduce tissue injury, organ dysfunction, and ultimately mortality due to hemorrhagic shock. Published 2018. Compr Physiol 8:61-101, 2018.

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Protective Effect of Estradiol on Acute Lung Inflammation Induced by an Intestinal Ischemic Insult is Dependent on Nitric Oxide

Cited by 47 publications

References 31 publications

Endothelial Progenitor Cells and a Stromal Cell–derived Factor-1α Analogue Synergistically Improve Survival in Sepsis

Endothelial Progenitor Cells and a Stromal Cell–derived Factor-1α Analogue Synergistically Improve Survival in Sepsis

Sex differences on solid organ histological characteristics after brain death1

Hemorrhagic Shock and the Microvasculature

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