Estrogen, NFκB, and the Heat Shock Response

Stice, James P.; Knowlton, Anne A

doi:10.2119/2008-00026.stice

Cited by 94 publications

(69 citation statements)

References 114 publications

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“…There are early estrogen effects, with rapid nongenomic activation of NFjB that are protective. A later response to bE2 results in the inhibition of NFjB, which is mediated by transcriptional, genomic effects [32]. In both B and T cells isolated from the spleen of C57Bl/6 mice, we could detect a rapid activation and nuclear translocation of p65 and p52 NFkB, while having no effect on cRel.…”

Section: Discussionmentioning

confidence: 70%

“…In both B and T cells isolated from the spleen of C57Bl/6 mice, we could detect a rapid activation and nuclear translocation of p65 and p52 NFkB, while having no effect on cRel. NFjB is a potent transcription factor that plays dual roles: its activation results in the expression of both pro-apoptotic and anti-apoptotic proteins as well as proinflammatory cytokines [32]. On the other hand, rapid NFjB activation also leads to cell proliferation and survival, while prolonged activation of NFjB may induce chronic inflammation.…”

Section: Discussionmentioning

confidence: 99%

“…Cellular signaling mechanisms activate the translocation of NFjB from cytoplasm to nucleus, which is required for NFjB to become a transcriptional regulator. Differential regulation of NFjB proteins by estrogen in spleen cells and in human T cells was recently reported [32,33]. We have tested whether in vitro treatment with bE2 can modulate subcellular distribution of NFjB in separated murine B and T lymphocytes by confocal laser scanning microscopy.…”

Section: Estrogen Induces Nfjb Activation and Ifnc Gene Transcriptionmentioning

confidence: 97%

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Estrogen augments the T cell-dependent but not the T-independent immune response

Ádori

Kiss

Barad

et al. 2010

Cell. Mol. Life Sci.

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Estrogen plays a critical regulatory role in the development and maintenance of immunity. Its role in the regulation of antibody synthesis in vivo is still not completely clear. Here, we have compared the effect of estrogen on T cell-dependent (TD) and T cell-independent type 2 (TI-2) antibody responses. The results provide the first evidence that estrogen enhances the TD but not the TI-2 response. Ovariectomy significantly decreased, while estrogen re-administration increased the number of hapten-specific IgM- and IgG-producing cells in response to TD antigen. In vitro experiments also show that estrogen may have a direct impact on B and T cells by inducing rapid signaling events, such as Erk and AKT phosphorylation, cell-specific Ca(2+) signal, and NFkappaB activation. These non-transcriptional effects are mediated by classical estrogen receptors and partly by an as yet unidentified plasma membrane estrogen receptor. Such receptor- mediated rapid signals may modulate the in vivo T cell-dependent immune response.

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Section: Discussionmentioning

confidence: 70%

Section: Discussionmentioning

confidence: 99%

Section: Estrogen Induces Nfjb Activation and Ifnc Gene Transcriptionmentioning

confidence: 97%

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Estrogen augments the T cell-dependent but not the T-independent immune response

Ádori

Kiss

Barad

et al. 2010

Cell. Mol. Life Sci.

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“…Nuclear factor-κB (NF-κB), a transcription factor of inflammatory genes, induces muscle atrophy, along with the loss of slow-twitch fibers (Li et al 2008, Wang & Pessin 2013. Estrogens suppress inflammation responses by inhibiting the activation of NF-κB (Stice & Knowlton 2008). Considering these findings, the effect of estrogen insufficiency on the properties of muscle might be involved in the activation of HIF1α and NF-κB in the muscle of our ovariectomy model.…”

Section: Discussionmentioning

confidence: 85%

Estrogens maintain skeletal muscle and satellite cell functions

Kitajima

Ono

2016

Journal of Endocrinology

120

115

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Estrogens have crucial roles in an extensive range of physiological functions regulating cellular proliferation and differentiation, development, homeostasis, and metabolism. Therefore, prolonged estrogen insufficiency influences various types of tissues expressing estrogen receptors (ERs). Although ERs are expressed in skeletal muscle and its stem cells, called satellite cells, how prolonged estrogen insufficiency affects their function remains unclear. In this study, we investigated the effect of estrogen reduction on muscle in young ovariectomized (OVX) female mice. We found that reduced estrogens resulted in muscle atrophy in a time-dependent manner. Muscle force generation was reduced in OVX mice. Interestingly, prolonged estrogen insufficiency shifted fiber types toward faster myosin heavy chain isoforms. The number of satellite cells per isolated myofiber was unchanged, while satellite cell expansion, differentiation, and self-renewal were all markedly impaired in OVX mice. Indeed, muscle regeneration was significantly compromised in OVX mice. Taken together, our results demonstrate that estrogens are essential for comprehensively maintaining muscle function with its insufficiency affecting muscle strength and regeneration in young female mice.

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“…2.1) (Straub, 2007). Additionally, there is much research on the ability of E2 and estrogen receptor α to regulate NFκB activity (Stice and Knowlton, 2008). Genomically, E2 is able to increase the expression of nuclear factor of kappa light polypeptide gene enhancer in B cells inhibitor, alpha (IkBα), the inhibitory subunit of NFκB (Fig.…”

Section: Anti-inflammatory Activity Of Estrogensmentioning

confidence: 99%

Estrogens, inflammation and obesity: an overview

et al. 2012

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Emerging research has suggested that inflammatory stress may play a role in the development of obesity. Both the leptin and insulin receptor are sensitive to intracellular inflammatory signaling that can be stimulated through toll-like receptor 4 activation by saturated fat. Pharmacological intervention within this cascade often protects animals from becoming obese, thus highlighting inflammatory pathways as a possible site of study in the prevention of pathologic weight gain. It has been well established in animal models that females display a marked reduction in the susceptibility to weight gain on high-fat diets compared to males. In addition, it has been widely accepted that females are partially protected from inflammatory-related diseases. At the molecular level, this reduction in disease susceptibility has been suggested to be due to the anti-inflammatory properties of 17 β-estradiol. Through direct free radical scavenging, transcriptional regulation, and protein interactions, chronic exposure to estradiol can reduce systemic inflammatory stress. As the knowledge base continues to grow on the etiology of obesity, further research is needed on the precise molecular pathways that can be inhibited by estradiol. Understanding of such pathways may provide a basis for the future use of estrogen and its related compounds (daidzein, genistein, resveratrol) to prevent weight gain in peri-and post-menopausal females.

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Estrogen, NFκB, and the Heat Shock Response

Cited by 94 publications

References 114 publications

Estrogen augments the T cell-dependent but not the T-independent immune response

Estrogen augments the T cell-dependent but not the T-independent immune response

Estrogens maintain skeletal muscle and satellite cell functions

Estrogens, inflammation and obesity: an overview

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