17<b>β</b>-Estradiol transcriptionally modulates Nlrp1 and Nlrp3 inflammasomes in gonadectomized rats with inflammation

López, Modesto Gómez; López, Aaron Domínguez; Rojano, Edgar Abarca; Rojas-Hernández, Saúl; Godinez, Maria de los Angeles Martinez; García, Ángel Miliar; Rodríguez, Rafael Campos

doi:10.3109/08923973.2015.1059439

Cited by 7 publications

(3 citation statements)

References 59 publications

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“…It is not clear whether ERα, GPR30/GPER1 signalling is directly involved in inflammasome regulation. In systemic inflammation and myeloid cells, a positive correlation between NLRP1 and NLRP3 expression/induction was observed, respectively . By following the published data, it appears that mainly ERβ signalling is crucial for transmitting the effects of E 2 on inflammasomes .…”

Section: Inflammasome Regulation In the Cns By Oestrogensupporting

confidence: 58%

“…At the beginning of this millennium, the first data were presented showing that E 2 diminishes IL‐1β activity by modulating CASP1 expression in the brain . Although such effects were repeatedly described in subsequent years, only recently was evidence presented for the renal tubular system, the heart, hepatocellular carcinoma cells, endometrium tissue, after systemic inflammation and, finally, the ischaemic brain indictating that E 2 mitigates or prevents pro‐inflammatory cytokine expression directly at the inflammasome level. In Table , data focusing on E 2 ‐mediated inflammasome regulation are summarised.…”

Section: Inflammasome Regulation In the Cns By Oestrogenmentioning

confidence: 99%

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Brain inflammasomes in stroke and depressive disorders: Regulation by oestrogen

Slowik

Lammerding

Hoffmann

et al. 2018

J Neuroendocrinology

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Neuroinflammation is a devastating pathophysiological process that results in brain damage and neuronal death. Pathogens, cell fragments and cellular dysfunction trigger inflammatory responses. Irrespective of the cause, inflammasomes are key intracellular multiprotein signalling platforms that sense neuropathological conditions. The activation of inflammasomes leads to the auto-proteolytic cleavage of caspase-1, resulting in the proteolysis of the pro-inflammatory cytokines interleukin (IL)1β and IL18 into their bioactive forms. It also initiates pyroptosis, a type of cell death. The two cytokines contribute to the pathogenesis in acute and chronic brain diseases and also play a central role in human aging and psychiatric disorders. Sex steroids, in particular oestrogens, are well-described neuroprotective agents in the central nervous system. Oestrogens improve the functional outcome after ischaemia and traumatic brain injury, reduce neuronal death in Parkinson's and Alzheimer's disease, as well as in amyotrophic lateral sclerosis, attenuate glutamate excitotoxicity and the formation of radical oxygen species, and lessen the spread of oedema after damage. Moreover, oestrogens alleviate menopause-related depressive symptoms and have a positive influence on depressive disorders probably by influencing growth factor production and serotonergic brain circuits. Recent evidence also suggests that inflammasome signalling affects anxiety- and depressive-like behaviour and that oestrogen ameliorates depression-like behaviour through the suppression of inflammasomes. In the present review, we highlight the most recent findings demonstrating that oestrogens selectively suppress the activation of the neuroinflammatory cascade in the brain in acute and chronic brain disease models. Furthermore, we aim to describe putative regulatory signalling pathways involved in the control of inflammasomes. Finally, we consider that psychiatric disorders such as depression also contain an inflammatory component that could be modulated by oestrogen.

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Section: Inflammasome Regulation In the Cns By Oestrogensupporting

confidence: 58%

Section: Inflammasome Regulation In the Cns By Oestrogenmentioning

confidence: 99%

Brain inflammasomes in stroke and depressive disorders: Regulation by oestrogen

Slowik

Lammerding

Hoffmann

et al. 2018

J Neuroendocrinology

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“…It is well known that estrogen modulates cytokine immune responses. 23,24 Macrophages express functional estrogen receptors and secrete TNF-α, IL-6, IL-10, and many other cytokines which regulate organ immune responses. 25 We therefore analyzed the effects of E2 on the mRNA and protein expression of inflammatory cytokines of RAW264.7 cells.…”

Section: Discussionmentioning

confidence: 99%

17β-estradiol modulates the viability, phenotype, endocytosis, and inflammatory cytokine expression of RAW264.7 macrophages

et al. 2016

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17β-estradiol (E2) is a female sex steroid hormone and exerts a pivotal role not only in female pregnancy but also in organ immune responses. Macrophages, as a kind of antigen-presenting cells, play an important influence on the cellular and humoral immune responses and also express the E2 receptor. In the present study, we explored the effects of E2 on the viability, endocytosis, surface molecule, and inflammatory cytokine expression of RAW264.7 macrophages. Results showed that E2 slightly increased the cell proliferation and endocytosis of RAW264.7 cells, while notably decreasing the mRNA and protein levels of inflammatory cytokines such as tumor necrosis factor (TNF)-α and monocyte chemoattractant protein-1 (MCP-1). As for the expression of surface molecules closely associated with the functions of macrophages, E2 significantly reduced the levels of CD40, CD80, and MHC-II. Interestingly, E2 reduced the levels of CD86 at low dose (10 nM and 1 nM), while enhancing its expression at high doses (1 μM and 0.1 μM). These results suggest that E2 may play an immuno-suppressive role in the inflammatory reactions and some autoimmune diseases partly by influencing the expressions of some important surface molecules and inflammatory cytokines of macrophages.

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Electroacupuncture inhibits NLRP3 inflammasome activation through CB2 receptors in inflammatory pain

Gao

Xiang

et al. 2018

Brain, Behavior, and Immunity

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17β-Estradiol transcriptionally modulates Nlrp1 and Nlrp3 inflammasomes in gonadectomized rats with inflammation

Cited by 7 publications

References 59 publications

Brain inflammasomes in stroke and depressive disorders: Regulation by oestrogen

Brain inflammasomes in stroke and depressive disorders: Regulation by oestrogen

17β-estradiol modulates the viability, phenotype, endocytosis, and inflammatory cytokine expression of RAW264.7 macrophages

Electroacupuncture inhibits NLRP3 inflammasome activation through CB2 receptors in inflammatory pain

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