Glial Fibrillary Acidic Protein: Regulation by Hormones, Cytokines, and Growth Factors

Laping, Nicholas J.; Teter, Bruce; Nichols, Nancy R.; Rozovsky, Irina; Finch, Caleb E.

doi:10.1111/j.1750-3639.1994.tb00841.x

Cited by 212 publications

(128 citation statements)

References 135 publications

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“…Although apoE is often increased by inflammatory stimuli, and this can be coordinate with upregulation of the canonical glial reactivity marker GFAP (Poirier et al, 1991;Laping et al, 1994a) (which was downregulated by ibuprofen in these mice (Lim et al, 2000)), in some inflammatory and neurodegenerative conditions apoE mRNA expression is not coordinately regulated with GFAP mRNA (Laping et al, 1994b;Schauwecker et al, 1998;Petegnief et al, 2001), including conditions related to amyloid plaques and AD (Shao et al, 1997;Zarow and Victoroff, 1998). In addition, apoE mRNA is uniquely downregulated by apoE and Ab proteins (Soulie et al, 1999;Yamauchi et al, 2003).…”

Section: Discussionmentioning

confidence: 99%

Ibuprofen Suppresses Interleukin-1β Induction of Pro-Amyloidogenic α1-Antichymotrypsin to Ameliorate β-Amyloid (Aβ) Pathology in Alzheimer's Models

Morita

Teter

Yang

et al. 2005

Neuropsychopharmacol

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Epidemiological and basic research suggests that nonsteroidal anti-inflammatory drugs (NSAIDs) should protect against the most common forms of Alzheimer's disease (AD). Ibuprofen reduces amyloid (Ab) pathology in some transgenic models, but the precise mechanisms remain unclear. Although some reports show select NSAIDs inhibit amyloid production in vitro, the possibility that in vivo suppression of amyloid pathology occurs independent of Ab production has not been ruled out. We show that ibuprofen reduced Ab brain levels in rats from exogenously infused Ab in the absence of altered Ab production. To determine whether ibuprofen inhibits proamyloidogenic factors, APPsw (Tg2576) mice were treated with ibuprofen for 6 months, and expression levels of the Ab and inflammation-related molecules a 1 antichymotrypsin (ACT), apoE, BACE1, and peroxisome proliferator-activated receptor g) (PPARg) were measured. Among these, ACT, a factor whose overexpression accelerates amyloid pathology, was reduced by ibuprofen both in vivo and in vitro. IL-1b, which was reduced in our animals by ibuprofen, induced mouse ACT in vitro. While some NSAIDs may inhibit Ab42 production, these observations suggest that ibuprofen reduction of Ab pathology may not be mediated by altered Ab42 production. We present evidence supporting the hypothesis that ibuprofen-dependent amyloid reduction is mediated by inhibition of an alternate pathway (IL-1b and its downstream target ACT).

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Section: Discussionmentioning

confidence: 99%

Ibuprofen Suppresses Interleukin-1β Induction of Pro-Amyloidogenic α1-Antichymotrypsin to Ameliorate β-Amyloid (Aβ) Pathology in Alzheimer's Models

Morita

Teter

Yang

et al. 2005

Neuropsychopharmacol

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“…54 The biochemical mechanisms involved in reactive astrocytic gliosis remain to be determined; however, one possible means is activation of dopamine and glutamate receptors on astrocytes leading to stimulation of adenylyl cyclase activity 55 and subsequent phosphorylation of transcription factors that bind to the cAMP response elements located on the GFAP promoter region. 56 By means of this interaction between astrocytes and neurons, 52,57 it is likely that astrocytic cells actively contribute to long-term neuronal changes in response to psychostimulant drugs. Whether these changes are indicative of neurotoxicity or neuroplasticity remains to be determined; however, further understanding of the mechanisms involved in reactive astrocytic gliosis may provide insight into whether such changes are associated with repair and reversal of neuronal damage associated with cocaine abuse.…”

Section: Structuralmentioning

confidence: 99%

Integrative proteomic analysis of the nucleus accumbens in rhesus monkeys following cocaine self-administration

2008

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The reinforcing effects and long-term consequences of cocaine self-administration have been associated with brain regions of the mesolimbic dopamine pathway, namely the nucleus accumbens (NAc). Studies of cocaine-induced biochemical adaptations in rodent models have advanced our knowledge; however, unbiased detailed assessments of intracellular alterations in the primate brain are scarce, yet essential, to develop a comprehensive understanding of cocaine addiction. To this end, two-dimensional difference in gel electrophoresis (2D-DIGE) was used to compare changes in cytosolic protein abundance in the NAc between rhesus monkeys selfadministering cocaine and controls. Following image normalization, spots with significantly differential image intensities (P < 0.05) were identified, excised, trypsin digested and analyzed by matrix-assisted laser-desorption ionization time-of-flight time-of-flight (MALDI-TOF-TOF). In total, 1098 spots were subjected to statistical analysis with 22 spots found to be differentially abundant of which 18 proteins were positively identified by mass spectrometry. In addition, approximately 1000 protein spots were constitutively expressed of which 21 proteins were positively identified by mass spectrometry. Increased levels of proteins in the cocaine-exposed monkeys include glial fibrillary acidic protein, syntaxin-binding protein 3, protein kinase C isoform, adenylate kinase isoenzyme 5 and mitochondrial-related proteins, whereas decreased levels of proteins included β-soluble N-ethylmaleimide-sensitive factor attachment protein and neural and non-neural enolase. Using a complimentary proteomics approach, the differential expression of phosphorylated proteins in the cytosolic fraction of these subjects was examined. Two-dimensional gel electrophoresis (2DGE) was followed by gel staining with Pro-Q Diamond phosphoprotein gel stain, enabling differentiation of approximately 150 phosphoprotein spots between the groups. Following excision and trypsin digestions, MALDI-TOF-TOF was used to confirm the identity of 15 cocaine-altered phosphoproteins. Significant increased levels were detected for γ-aminobutyric acid type A receptor-associated protein 1, 14-3-3 γ-protein, glutathione S-transferase and brain-type aldolase, whereas significant decreases were observed for β-actin, Rab GDP-dissociation inhibitor, guanine deaminase, peroxiredoxin 2 isoform b and Results from these studies indicate coordinated dysregulation of proteins related to cell structure, signaling, metabolism and mitochondrial function. These data extend and compliment previous studies of cocaine-induced biochemical alterations in human post-mortem brain tissue, using an animal model that closely recapitulates the human condition and provide new insight into the molecular basis of the disease and potential targets for pharmacotherapeutic intervention.

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“…Oestradiol also promotes differentiation of glial cells with a redistribution of GFAP in hypothalamic astrocytes (Torres-Aleman et al 1992, Mong & Blutstein 2006. In addition, the transforming growth factor b has been reported to inhibit astrocyte proliferation and to induce the expression of GFAP in vivo (Reilly et al 1998, Sousa et al 2004) and in vitro (Laping et al 1994). Treatment with GHRP-6 did not increase GFAP levels but stimulated proliferation in the hypothalamus and hippocampus.…”

Section: Discussionmentioning

confidence: 95%

“…GFAP has been widely recognised as an astrocyte differentiation marker constituting the major intermediate filament protein of mature astrocyte (Galou et al 1996, Freeman 2010. Modulators of GFAP expression include steroids, cytokines and growth factors (Laping et al 1994, García-Segura & McCarthy 2004. Overexpression of GH in transgenic mice increases GFAP levels (Miller et al 1995).…”

Section: Discussionmentioning

confidence: 99%

Differential effects of GH and GH-releasing peptide-6 on astrocytes

Baquedano¹,

Chowen²,

Argente³

et al. 2013

Journal of Endocrinology

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GH and GH secretagogues (GHSs) are involved in many cellular activities such as stimulation of mitosis, proliferation and differentiation. As astrocytes are involved in developmental and protective functions, our aim was to analyse the effects of GH and GH-releasing hexapeptide on astrocyte proliferation and differentiation in the hypothalamus and hippocampus. Treatment of adult male Wistar rats with GH (i.v., 100 mg/day) for 1 week increased the levels of glial fibrillary acidic protein (GFAP) and decreased the levels of vimentin in the hypothalamus and hippocampus. These changes were not accompanied by increased proliferation. By contrast, GH-releasing hexapeptide (i.v., 150 mg/day) did not affect GFAP levels but increased proliferation in the areas studied. To further study the intracellular mechanisms involved in these effects, we treated C6 astrocytoma cells with GH or GH-releasing hexapeptide and the phosphatidylinositol 3 0 -kinase (PI3K) inhibitor, LY294002, and observed that the presence of this inhibitor reverted the increase in GFAP levels induced by GH and the proliferation induced by GH-releasing hexapeptide. We conclude that although GH-releasing hexapeptide is a GHS, it may exert GH-independent effects centrally on astrocytes when administered i.v., although the effects of both substances appear to be mediated by the PI3K/Akt pathway.

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Glial Fibrillary Acidic Protein: Regulation by Hormones, Cytokines, and Growth Factors

Cited by 212 publications

References 135 publications

Ibuprofen Suppresses Interleukin-1β Induction of Pro-Amyloidogenic α1-Antichymotrypsin to Ameliorate β-Amyloid (Aβ) Pathology in Alzheimer's Models

Ibuprofen Suppresses Interleukin-1β Induction of Pro-Amyloidogenic α1-Antichymotrypsin to Ameliorate β-Amyloid (Aβ) Pathology in Alzheimer's Models

Integrative proteomic analysis of the nucleus accumbens in rhesus monkeys following cocaine self-administration

Differential effects of GH and GH-releasing peptide-6 on astrocytes

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