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PI3K‐R1 expression in hepatic tissue of horses with laminitis
Author(s) -
Carlisle Katherine,
McGeachy Matthew,
Garza Frank,
Stokes Ashley Michelle
Publication year - 2009
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.23.1_supplement.929.2
Subject(s) - laminitis , pi3k/akt/mtor pathway , biology , pathogenesis , real time polymerase chain reaction , medicine , horse , endocrinology , pathology , microbiology and biotechnology , signal transduction , gene , biochemistry , paleontology
Phosphatidylinositol‐3‐Kinase (PI3K) is an inhibitor of pro‐inflammatory processes regulated by two converging pathways. It is a cytoplasmic component of the Toll‐Like Receptor Signaling Pathway and is also affected by insulin receptor activation. The objective was to examine gene expression of the regulatory subunit p85 (R1) of PI3K in equine liver samples from normal (n=13), naturally acquired laminitis (n=11), experimentally induced laminitis (n=7), and metabolic disorder (n=3) cases. Total cellular RNA was extracted, analyzed by agarose gel electrophoresis, quantified by spectrophotometry, reverse transcribed to cDNA, and quantified by TaqMan RT‐PCR. The most significant finding of this study was a difference between PI3K expression and laminitis activity (p=0.0441). Horses with active cases of laminitis, Obel grade ¡Ý 1, demonstrated significantly less expression of PI3K than horses with inactive cases (fold decrease=10.26). We also found a marked increase of PI3K in horses with metabolic disorders compared to those with laminitis (fold increase=14.949). Our study suggests a relationship may exist between PI3K down‐regulation and the pathogenesis of laminitis. Therefore, PI3K‐R1 deserves further investigation as an inflammatory mediator that can be targeted in prevention and treatment of laminitis. Funding provided by the LSU Equine Health Studies Program.