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Am J Physiol Cell Physiol (September 19, 2007). doi:10.1152/ajpcell.00554.2006
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Submitted on October 30, 2006
Accepted on September 12, 2007

ACTIVITY-DEPENDENT NFATc3 NUCLEAR ACCUMULATION IN PERICYTES FROM CORTICAL PARENCHYMAL MICROVESSEL

Jessica Andrea Filosa1*, Mark T Nelson2, and Laura V Gonzalez Bosc3

1 Psychiatry, University of Cincinnati, Cincinnati, Ohio, United States
2 Pharmacology, University of Vermont, Burlington, Vermont, United States
3 Cell Biology and Physiology, University of New Mexico, Albuquerque, New Mexico, United States

* To whom correspondence should be addressed. E-mail: jessica.filosa{at}uc.edu.

The calcium-dependent transcription factor, NFATc3, is critical for embryonic vascular development and differentiation. Despite its potential importance, nothing is known about NFATc3 regulation in the brain microcirculation. In this study, we sought to investigate the role 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 t-ACPD. NFATc3, glial fibrillary acidic protein (GFAP, astrocytic specific marker) and platelet-derived growth factor {beta}-receptor (PDGF-{beta} 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 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 inhibition of calcineurin, cyclooxygenase and nitric oxide synthase. This is the first study to report NFATc3 expression in pericytes from parenchymal microvessels and 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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