| Activity-dependent NFATc3 nuclear accumulation in pericytes from cortical parenchymal microvessels. | |
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MedLine Citation:
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PMID: 17881610 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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The calcium-dependent transcription factor NFATc3, which is a member of the nuclear factor of activated T cells (NFAT) family of transcription factors, is critical for embryonic vascular development and differentiation. Despite its potential importance, nothing is known about NFATc3 regulation in the brain microcirculation. In the present study, we sought to investigate the role that glutamate, possibly through astrocytic communication, plays in the control of NFATc3 regulation in pericytes from parenchymal microvessels. Coronal cortical slices from neonatal rats were subjected to electrical field stimulation or were treated with the metabotropic glutamate receptor agonist (+/-)-1-aminocyclopentane-trans-1,3-dicarboxylic acid (t-ACPD). NFATc3, glial fibrillary acidic protein (an astrocyte-specific marker), and platelet-derived growth factor-beta-receptor (a pericyte-specific marker) were detected by immunofluorescence. Electrical field stimulation induced NFATc3 nuclear accumulation in pericytes. This response was dependent on neuronal activity and group I metabotropic glutamate receptor (mGluR) activation. In addition, t-ACPD significantly increased NFATc3 nuclear accumulation in both astrocytes and pericytes. NFATc3 nuclear accumulation in pericytes was prevented when astrocytic function was abolished with the gliotoxin L-alpha-aminoadipate or by the inhibition of calcineurin, cyclooxygenase, and nitric oxide synthase. This is the first study to report NFATc3 expression in pericytes from parenchymal microvessels and in astrocytes from native tissue. Our results suggest a model by which glutamate, via mGluR activation, may regulate gene transcription in pluripotent vascular pericytes. |
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Authors:
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Jessica A Filosa; Mark T Nelson; Laura V Gonzalez Bosc |
Publication Detail:
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Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't Date: 2007-09-19 |
Journal Detail:
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Title: American journal of physiology. Cell physiology Volume: 293 ISSN: 0363-6143 ISO Abbreviation: Am. J. Physiol., Cell Physiol. Publication Date: 2007 Dec |
Date Detail:
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Created Date: 2007-12-12 Completed Date: 2008-03-04 Revised Date: - |
Medline Journal Info:
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Nlm Unique ID: 100901225 Medline TA: Am J Physiol Cell Physiol Country: United States |
Other Details:
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Languages: eng Pagination: C1797-805 Citation Subset: IM |
Affiliation:
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Department of Psychiatry, University of Cincinnati, Cincinnati, OH 45237, USA. jessica.filosa@uc.edu |
Export Citation:
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| MeSH Terms | |
Descriptor/Qualifier:
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Animals Animals, Newborn Astrocytes / metabolism, physiology* Cell Nucleus / metabolism* Cerebral Cortex / blood supply Electric Stimulation Gene Expression Regulation Glutamic Acid / metabolism* NFATC Transcription Factors / metabolism* Pericytes / metabolism* Rats Rats, Sprague-Dawley Receptors, Metabotropic Glutamate / agonists Signal Transduction / physiology |
| Grant Support | |
ID/Acronym/Agency:
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DK53832/DK/NIDDK NIH HHS; HL44455/HL/NHLBI NIH HHS; HL63722/HL/NHLBI NIH HHS |
| Chemical | |
Reg. No./Substance:
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0/NFATC Transcription Factors; 0/Receptors, Metabotropic Glutamate; 0/transcription factor NF-AT c3; 56-86-0/Glutamic Acid |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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