Immunoreactivity for glial fibrillary acidic protein and P2 receptor expression on astrocytes in vivo

2003 ◽  
Vol 59 (1) ◽  
pp. 175-189 ◽  
Author(s):  
Heike Franke ◽  
Ute Krügel ◽  
Jens Grosche ◽  
Peter Illes
Keyword(s):  
Glial Fibrillary Acidic Protein ◽  
Receptor Expression ◽  
Acidic Protein ◽  
P2 Receptor

The immunoreactivity of glial fibrillary acidic protein in mesangial cells and podocytes of the glomeruli of rat kidney in vivo and in culture

1998 ◽  
Vol 90 (1) ◽  
pp. 53-61 ◽  
Author(s):  
Gayane Buniatian ◽  
Peter Traub ◽  
Margitta Albinus ◽  
Gerhard Beckers ◽  
Albrecht Buchmann ◽  
...  
Keyword(s):  
Glial Fibrillary Acidic Protein ◽  
Mesangial Cells ◽  
Rat Kidney ◽  
Acidic Protein

Indicator expression directed by regulatory sequences of the glial fibrillary acidic protein (GFAP) gene: In vivo comparison of distinct GFAP-lacZ transgenes

Glia ◽  
1995 ◽  
Vol 13 (3) ◽  
pp. 174-184 ◽  
Author(s):  
William B. Johnson ◽  
Mary D. Ruppe ◽  
Edward M. Rockenstein ◽  
Jennifer Price ◽  
Vijay P. Sarthy ◽  
...  
Keyword(s):  
Glial Fibrillary Acidic Protein ◽  
Acidic Protein ◽  
Regulatory Sequences

Glial fibrillary acidic protein - a cell type specific marker for Ito cells in vivo and in vitro

1996 ◽  
Vol 24 (6) ◽  
pp. 719-730 ◽  
Author(s):  
Katrin Neubauer ◽  
Thomas Knittel ◽  
Sabine Aurisch ◽  
Peter Fellmer ◽  
Giuliano Ramadori
Keyword(s):  
Glial Fibrillary Acidic Protein ◽  
Protein A ◽  
Acidic Protein ◽  
Specific Marker ◽  
Cell Type ◽  
Ito Cells ◽  
A Cell ◽  
Cell Type Specific

Glial fibrillary acidic protein mRNA isotypes: Expression in vitro and in vivo

1995 ◽  
Vol 41 (4) ◽  
pp. 452-461 ◽  
Author(s):  
E. Galea ◽  
P. Dupouey ◽  
D. L. Feinstein
Keyword(s):  
Glial Fibrillary Acidic Protein ◽  
Acidic Protein

scholarly journals Induction of gp130-related Cytokines and Activation of JAK2/STAT3 Pathway in Astrocytes Precedes Up-regulation of Glial Fibrillary Acidic Protein in the 1-Methyl-4-phenyl-1,2,3,6-tetrahydropyridine Model of Neurodegeneration

2004 ◽  
Vol 279 (19) ◽  
pp. 19936-19947 ◽  
Author(s):  
Krishnan Sriram ◽  
Stanley A. Benkovic ◽  
Meleik A. Hebert ◽  
Diane B. Miller ◽  
James P. O'Callaghan
Keyword(s):  
Glial Fibrillary Acidic Protein ◽  
Signaling Pathway ◽  
Janus Kinase ◽  
Acidic Protein ◽  
Oncostatin M ◽  
Nerve Terminals ◽  
Stat3 Signaling ◽  
Stat3 Signaling Pathway ◽  
Stat Pathway

Reactive gliosis is a hallmark of disease-, trauma-, and chemical-induced damage to the central nervous system. The signaling pathways associated with this response to neural injury remain to be elucidated, but recent evidence implicates the Janus kinase (JAK)-signal transducer and activator of transcription (STAT) pathway. Here, we used the known dopaminergic neurotoxicant, 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP), to selectively damage striatal dopaminergic nerve terminals and elicit a glial response. We then analyzed changes in gene expression and protein phosphorylation,in vivo, to identify ligands and mediators of the JAK-STAT pathway that accompany glial activation. Administration of MPTP caused rapid tyrosine (Tyr-705) phosphorylation and nuclear translocation of STAT3 in striatal astrocytes, prior to the induction of glial fibrillary acidic protein mRNA and protein. Pharmacological protection of dopaminergic nerve terminals with nomifensine abolished MPTP-mediated phosphorylation and translocation of STAT3 and prevented induction of astrogliosis. Among the Janus kinase family of tyrosine kinases, only JAK2 was associated with the phosphorylation of STAT3 after MPTP and, inhibition of JAK2 by AG490,in vivo, attenuated both the phosphorylation of STAT3 and induction of GFAP. The p44/42 mitogen-activated protein kinase (MAPK; ERK1/2) also was activated by MPTP, but was not associated with activation of STAT3, because serine (Ser-727) was not phosphorylated. The mRNA for ligands of the gp130-JAK/STAT3 signaling pathway, interleukin-6, leukemia inhibitory factor, and oncostatin M were elevated prior to activation of STAT3 and induction of astrogliosis; neuroprotection with nomifensine blocked these effects of MPTP. Taken together, our results suggest that the gp130-mediated activation of JAK2/STAT3 signaling pathway may play a key role in the induction of astrogliosis.

scholarly journals Estradiol (E2) Enhances Neurite Outgrowth by Repressing Glial Fibrillary Acidic Protein Expression and Reorganizing Laminin

Endocrinology ◽  
2002 ◽  
Vol 143 (2) ◽  
pp. 636-646 ◽  
Author(s):  
Irina Rozovsky ◽  
Min Wei ◽  
David J. Stone ◽  
Hadi Zanjani ◽  
Christopher P. Anderson ◽  
...  
Keyword(s):  
Glial Fibrillary Acidic Protein ◽  
Neurite Outgrowth ◽  
Enhanced Recovery ◽  
Acidic Protein ◽  
Female Rats ◽  
Upstream Region ◽  
Transcriptional Responses ◽  
Neuronal Remodeling ◽  
Gfap Expression

Abstract Neuronal remodeling in response to deafferenting lesions in the brain can be enhanced by estradiol (E2). Astrocytes are among the targets of E2 in complex interactions with neurons and may support or inhibit neuronal remodeling. In ovariectomized female rats given entorhinal cortex lesions, E2 replacement inhibited the increase of glial fibrillary acidic protein (GFAP) protein. To model the role of E2 in these complex processes, we used the “wounding-in-a-dish” of astrocyte-neuron cocultures. Low physiological E2 (1 pm) blocks the wound-induced increase of GFAP expression (transcription and protein) and enhances neurite outgrowth. The transcriptional responses to E2 during wounding are mediated by sequences in the 5′-upstream region of the rat GFAP promoter. Concurrently, E2 reorganized astrocytic laminin into extracellular fibrillar arrays, which others have shown support neurite outgrowth. The inhibition of GFAP expression by E2 in this model is consistent with in vivo findings that E2 enhanced recovery from deafferenting cortical lesions by increased neurite outgrowth in association with decreased GFAP expression. More generally, we hypothesize that physiological variations in E2 levels modulate neuronal plasticity through direct effects on GFAP transcription that, in turn, modify GFAP-containing intermediate filaments and reorganize astrocytic laminin.

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