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Expression and distribution of the scavenger receptor CD36 suggests important roles in the pathophysiology of spinal cord injury (729.3)
Author(s) -
CorderoCabán Kathia,
LiceroCampbell Jennifer,
Figueroa Johnny,
De León Marino
Publication year - 2014
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.28.1_supplement.729.3
Subject(s) - cd36 , spinal cord , medicine , spinal cord injury , pathophysiology , scavenger receptor , neurodegeneration , inflammation , receptor , context (archaeology) , neuroscience , endocrinology , biology , disease , cholesterol , lipoprotein , paleontology
Spinal cord injury (SCI) remains a devastating cause of lifetime medical comorbidities in modern society. Unfortunately, only a few preventive strategies have been shown to prevent the profound pathophysiological mechanisms associated with this condition. In previous studies, our laboratory has shown that a diet enriched in polyunsaturated fatty acids (O3PUFAs), including docosahexaenoic acid (DHA), can reduce neurodegeneration, chronic pain, motor functional deficit, loss of sensitivity, and accelerates autonomic bladder function in a rat model of SCI. CD36 is a multifunctional protein that has been recently implicated as a scavenger receptor and lipid transporter. This membrane protein plays a major role in physiological and pathological inflammation. The purpose of this study was to investigate the expression and roles of CD36 in the context of SCI and dietary O3PUFAs. We hypothesized that trauma to the spinal cord result in a reduction in the protein levels of this protein. Further, we proposed that dietary O3PUFAs normalize the expression of CD36 in the injured spinal cord. Here we determined the protein expression of CD36 after SCI. In particular, we analyzed the temporal and spatial expression of CD36 after contusive injury to the rat spinal cord using immunoblotting and double‐labeling immunofluorescent experiments. Our data demonstrates that acute SCI results in a marked downregulation of CD36. This protein was predominantly observed in both neuronal and glial cells. Importantly, we found that dietary lipids may be implicated in the regulation of this important protein. Altogether, our data supports a potential molecular link between dietary O3PUFAs beneficial effects in the injured spinal cord. This protein may represent an important therapeutic target to reduce the burden of SCI in humans. Grant Funding Source : Supported by 5P20MD006988 and 2R25GM060507