role of estrogen receptors in the regulation of reactive gliosis

Clicks: 349
ID: 182364
2015
Free PDF
Article Quality & Performance Metrics
Overall Quality
Not rated
Combines reader engagement with the AI quality analysis. This article has not been analysed, so there is no overall score — reader engagement is measured and shown alongside.
AI Quality Assessment
Not analyzed
Readership in this journal
Steady

Ranked #24 of 394 articles by views in macromolecular bioscience

Most read Least read

Bar heights use a square-root scale. Only the 120 most-read articles are drawn; the journal has 394 in total.

Mint this article as an NFT
Not yet minted

Create a permanent, verifiable on-chain record of this article on the Scimatic Network. The NFT is held in your Journament account, and you can withdraw it to your own wallet at any time.

5 SUSD one-off · no wallet required
Sign in to mint
Abstract
Although estradiol may directly act on neurons to promote neuroprotection in vitro, the participation of other cell types is also necessary to maintain global tissue homeostasis in vivo (Arevalo et al., 2010; Johann and Beyer, 2013; Acaz-Fonseca et al., 2014). Thus, estradiol acts on glial and endothelial cells to maintain the function of the neurovascular unit, regulates gliosis and the inflammatory response of astrocytes and microglia to control neuroinflammation and acts on neurons, astrocytes and oligodendrocytes to maintain the function and propagating properties of neuronal circuits (Garcia-Ovejero et al., 2005; Tapia-Gonzalez et al., 2008; Barrerto et al., 2009; Cerciat et al., 2010; López Rodríguez et al., 2011; Barreto et al., 2014). Glial cells express estrogen receptors (ERs), including ERalpha, ERbeta and G protein-coupled estrogen receptor-1 (GPER) (Garcia-Ovjero et al., 2005; Dhandapani and Brann, 2007) and brain injury induces both the synthesis of estradiol in both reactive astrocytes and the expression of ERs in these cells (Garcia-Ovejero et al., 2002). This suggests that astrocytes may play an important role in the neuroprotective actions of estradiol. Indeed, recent studies, using conditional KO mice for ERalpha and ERbeta, have shown that in an experimental model of multiple sclerosis the protective action of estradiol is mediated by ERalpha expressed in astrocytes, but not by ERalpha expressed in neurons or ERbeta expressed in astrocytes or neurons (Spence et al., 2013). ERs in glial cells activate several neuroprotective mechanisms in response to estradiol, including the release of factors that have trophic effects on neurons and other cell types and the control of neuroinflammation, edema and extracellular glutamate levels. Classical ERs associated with the plasma membrane of astrocytes are involved in the estradiol-induced release of transforming growth factor (TGF)-beta, through the activation of the PI3K/Akt signaling pathway (Sortino et al., 2004; Dhandapani et al., 2005). In addition, both ERalpha and ERbeta are involved in the anti-inflammatory and anti-gliotic actions of estradiol on microglia and astrocytes (Vegeto et al., 2003; Liu et al., 2005). The anti-inflammatory action of ERalpha is also exerted through the activation of the PI3K pathway, which in turns blocks nuclear factor kB (NFkB) activation and translocation to the cell nucleus (Ghisletti et al., 2005). ERbeta also plays an essential role in the regulation of the neuroinflammatory response of astrocytes. This effect is in part mediated by the upregulation of neuroglobin (De Marinis et al., 2013), a hemoprotein with partial sequence identity with vertebrate hemoglobin and myoglobin, which protects neurons from a variety of insults, such as hypoxia, glucose deprivation, oxidative stress, beta-amyloid toxicity and experimental stroke.
Reference Key
garcia-segura2015frontiersrole Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors ;Luis Miguel Garcia-Segura;Inigo Azcoitia;George E. Barreto
Journal macromolecular bioscience
Year 2015
DOI
10.3389/conf.fncel.2015.35.00001
URL
http://journal.frontiersin.org/Journal/10.3389/conf.fncel.2015.35.00001/full
Keywords
microglia astrocytes estradiol neuroglobin aromatase neuropsychiatry biological psychiatry

Citations

No citations found. To add a citation, contact the admin at info@scimatic.org

Comments

No comments yet. Be the first to comment on this article.