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Transient Increase in P2Y2 Receptor Expression after Spinal Cord Injury in Rat Model
Author(s) -
Rodríguez Ana E.,
Torrado Aranza,
Figueroa Johnny D.,
González Fernando A.,
Miranda Jorge D.
Publication year - 2008
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.22.1_supplement.1231.7
Subject(s) - astrogliosis , spinal cord injury , immunohistochemistry , spinal cord , receptor , astrocyte , microbiology and biotechnology , biology , gene expression , pathology , chemistry , medicine , neuroscience , central nervous system , immunology , gene , biochemistry
Spinal cord injury (SCI) increases inhibitory molecules release and reactive astrocytes proliferation at injury site producing nonpermissive environment for axonal regeneration. Reactive astrogliosis mechanism is unknown, but the release of nucleotides has been linked to this hypertrophic state. Our goal is to investigate the spatio‐temporal profile of P2Y 2 after SCI. Molecular biology and immunohistochemical (IHC) studies were used to evaluate the expression and role of these receptors in rats injured at the T‐10 level using the NYU impactor device. P2Y 2 gene temporal profile using standardized RT‐PCR showed a two‐fold increase after 4–7 days post‐injury (DPI) and returned to basal levels by 14 DPI. Double labeling IMH localized P2Y 2 in cells bodies, axons, macrophages, oligodendrocytes and astrocytes. Also, levels of P2Y 2 immunoreactivity were increased after injury in astrocytes. Therefore, the gene profile of P2Y2 after SCI showed that the levels of this mRNA and protein increased after trauma, suggesting a role in the establishment of the restrictive environment for axonal regeneration after SCI. Support by NIH‐MRISP 2R2MH48190‐14, NIH‐SNRP NS39405, MBRS‐SCORE S06‐ GM008224 , MBRS‐RISE GM‐68138, PR‐EPSCOR EPS‐9874782