Short- and long-term treatment with estradiol or progesterone modifies the expression of GFAP, MAP2 and Tau in prefrontal cortex and hippocampus

González-Arenas, Aliesha; Espinosa-Raya, Judith; Piña-Medina, Ana Gabriela; Picazo, Ofir Picazo

doi:10.1016/j.lfs.2011.05.008

Cited by 14 publications

(12 citation statements)

References 71 publications

(77 reference statements)

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“…For instance, we found that the expression of mERα at the cell surface, occurring after CMP, was associated with the expression of the MAP2 cytoskeletal protein, known to be involved in microtubule assembly and neurogenesis [29]. We cannot rule out the possibility that MAP2 phosphorylation and overexpression, previously observed in E2-treated hippocampal cells [35]–[37], could play a role in CMP-associated mERα expression at the cell surface. Conversely, actin microfilaments, although partially rearranged in CMP-treated neuronal cells, did not display any overlay with mERα expression, so that a role for actin filaments in mERα up-regulation should be ruled out.…”

Section: Discussionmentioning

confidence: 67%

Cell Surface Estrogen Receptor Alpha Is Upregulated during Subchronic Metabolic Stress and Inhibits Neuronal Cell Degeneration

et al. 2012

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In addition to the classical nuclear estrogen receptor, the expression of non-nuclear estrogen receptors localized to the cell surface membrane (mER) has recently been demonstrated. Estrogen and its receptors have been implicated in the development or progression of numerous neurodegenerative disorders. Furthermore, the pathogenesis of these diseases has been associated with disturbances of two key cellular programs: apoptosis and autophagy. An excess of apoptosis or a defect in autophagy has been implicated in neurodegeneration. The aim of this study was to clarify the role of ER in determining neuronal cell fate and the possible implication of these receptors in regulating either apoptosis or autophagy. The human neuronal cell line SH-SY5Y and mouse neuronal cells in primary culture were thus exposed to chronic minimal peroxide treatment (CMP), a form of subcytotoxic minimal chronic stress previously that mimics multiple aspects of long-term cell stress and represents a limited molecular proxy for neurodegenerative processes. We actually found that either E2 or E2-bovine serum albumin construct (E2BSA, i.e. a non-permeant form of E2) was capable of modulating intracellular cell signals and regulating cell survival and death. In particular, under CMP, the up-regulation of mERα, but not mERβ, was associated with functional signals (ERK phosphorylation and p38 dephosphorylation) compatible with autophagic cytoprotection triggering and leading to cell survival. The mERα trafficking appeared to be independent of the microfilament system cytoskeletal network but was seemingly associated with microtubular apparatus network, i.e., to MAP2 molecular chaperone. Importantly, antioxidant treatments, administration of siRNA to ERα, or the presence of antagonist of ERα hindered these events. These results support that the surface expression of mERα plays a pivotal role in determining cell fate, and that ligand-induced activation of mER signalling exerts a powerful cell-survival signal. These results shed new light on the pathogenetic mechanisms leading to neuronal cell degeneration.

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Section: Discussionmentioning

confidence: 67%

Cell Surface Estrogen Receptor Alpha Is Upregulated during Subchronic Metabolic Stress and Inhibits Neuronal Cell Degeneration

et al. 2012

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“…Progesterone itself has neurobiological actions unique from those of progestins, including neurotrophic and neuroprotective effects in animal models, however there is little known about the potential effects of progesterone on postmenopausal cognition (Pluchino et al, 2009; Schussler et al, 2008). Progesterone has been shown to modulate cognitive function in aging rats through actions in the hippocampus and prefrontal cortex (Camacho-Arroyo et al, 2011; Frye and Walf, 2008; Paris et al, 2011). While there is ample evidence for estrogenic regulation of prefrontal dendritic spine density, progesterone mechanisms in this region are less clear.…”

Section: Discussionmentioning

confidence: 99%

“…While there is ample evidence for estrogenic regulation of prefrontal dendritic spine density, progesterone mechanisms in this region are less clear. A study in ovariectomized rats found that 18 weeks of progesterone, but not estradiol, increased expression of glial fibrillary acidic protein and microtubule-associated proteins, which are associated with neurotrophic actions including neuronal transport and plasticity as well as dendrite stability and extension (Camacho-Arroyo et al, 2011). …”

Section: Discussionmentioning

confidence: 99%

Distinct cognitive effects of estrogen and progesterone in menopausal women

Berent-Spillson

Briceño

Pinsky

et al. 2015

Psychoneuroendocrinology

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The effects of postmenopausal hormone treatment on cognitive outcomes are inconsistent in the literature. Emerging evidence suggests that cognitive effects are influenced by specific hormone formulations, and that progesterone is more likely to be associated with positive outcomes than synthetic progestin. There are very few studies of unopposed progesterone in postmenopausal women, and none that use functional neuroimaging, a sensitive measure of neurobiological function. In this study of 29 recently postmenopausal women, we used functional MRI and neuropsychological measures to separately assess the effects of estrogen or progesterone treatment on visual and verbal cognitive function. Women were randomized to receive 90 days of either estradiol or progesterone counterbalanced with placebo. After each treatment arm, women were given a battery of verbal and visual cognitive function and working memory tests, and underwent functional MRI including verbal processing and visual working memory tasks. We found that both estradiol and progesterone were associated with changes in activation patterns during verbal processing. Compared to placebo, women receiving estradiol treatment had greater activation in the left prefrontal cortex, a region associated with verbal processing and encoding. Progesterone was associated with changes in regional brain activation patterns during a visual memory task, with greater activation in the left prefrontal cortex and right hippocampus compared to placebo. Both treatments were associated with a statistically nonsignificant increase in number of words remembered following the verbal task performed during the fMRI scanning session, while only progesterone was associated with improved neuropsychological measures of verbal working memory compared to placebo. These results point to potential cognitive benefits of both estrogen and progesterone.

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“…Furthermore, sex steroids also have dramatic effect on GFAP expression. One example is that GFAP expression was diminished in rat hippocampus after chronic administration of progesterone (Camacho‐Arroyo, Gonzalez‐Arenas, Espinosa‐Raya, Pina‐Medina, & Picazo, ). Clearly, reproduction‐associated hormones are important regulators of GFAP expression.…”

Section: Expression Of Gfap and Its Regulationmentioning

confidence: 99%

Neurochemical regulation of the expression and function of glial fibrillary acidic protein in astrocytes

Liu

et al. 2019

Glia

117

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Glial fibrillary acidic protein (GFAP), a type III intermediate filament, is a marker of mature astrocytes. The expression of GFAP gene is regulated by many transcription factors (TFs), mainly Janus kinase‐2/signal transducer and activator of transcription 3 cascade and nuclear factor κ‐light‐chain‐enhancer of activated B cell signaling. GFAP expression is also modulated by protein kinase and other signaling molecules that are elicited by neuronal activity and hormones. Abnormal expression of GFAP proteins occurs in neuroinflammation, neurodegeneration, brain edema‐eliciting diseases, traumatic brain injury, psychiatric disorders and others. GFAP, mainly in α‐isoform, is the major component of cytoskeleton and the scaffold of astrocytes, which is essential for the maintenance of astrocytic structure and shape. GFAP also has highly morphological plasticity because of its quick changes in assembling and polymerizing states in response to environmental challenges. This plasticity and its corresponding cellular morphological changes endow astrocytes the functions of physical barrier between adjacent neurons and stabilizer of extracellular environment. Moreover, GFAP colocalizes and even molecularly associates with many functional molecules. This feature allows GFAP to function as a platform for direct interactions between different molecules. Last, GFAP involves transportation and localization of other functional proteins and thus serves as a protein transport guide in astrocytes. This guiding role of GFAP involves an elastic retraction and extension cytoskeletal network that couples with GFAP reassembling, transporting, and membrane protein recycling machinery. This paper reviews our current understanding of the expression and functions of GFAP as well as their regulation.

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Short- and long-term treatment with estradiol or progesterone modifies the expression of GFAP, MAP2 and Tau in prefrontal cortex and hippocampus

Cited by 14 publications

References 71 publications

Cell Surface Estrogen Receptor Alpha Is Upregulated during Subchronic Metabolic Stress and Inhibits Neuronal Cell Degeneration

Cell Surface Estrogen Receptor Alpha Is Upregulated during Subchronic Metabolic Stress and Inhibits Neuronal Cell Degeneration

Distinct cognitive effects of estrogen and progesterone in menopausal women

Neurochemical regulation of the expression and function of glial fibrillary acidic protein in astrocytes

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