Abstract
Lysophosphatidic acid (LPA) is involved in physiological and pathological states, including in neural development and inflammation. We assessed the expression pattern of the LPA receptors 1-3 and of LPA-producing enzyme autotaxin in post-mortem human brain tissue, both in normal individuals and in individuals who died following traumatic brain injury. We found that LPA receptors and autotaxin are weakly expressed in the normal control adult brain. Quantitative PCR for the LPA receptors and autotaxin mRNA showed an increase of LPAR(2) and a decrease of autotaxin mRNA expression in the cortex following brain injury. Immunohistochemical analysis showed that LPAR(1) colocalized with astrocytes and that LPAR(2) is present on the ependymal cells lining the lateral ventricle in the brain samples from individuals who died following severe head injury. This work shows for the first time that key components of the LPA pathway are modulated following TBI in humans.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Adolescent
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Adult
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Aged
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Antibody Specificity / immunology
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Astrocytes / metabolism
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Astrocytes / pathology
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Brain / metabolism*
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Brain / pathology*
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Brain Injuries / genetics*
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Brain Injuries / pathology*
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Ependyma / metabolism
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Ependyma / pathology
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Female
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Gene Expression Regulation
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Humans
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Male
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Middle Aged
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Multienzyme Complexes / genetics
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Multienzyme Complexes / metabolism
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Phosphodiesterase I / genetics
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Phosphodiesterase I / metabolism
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Phosphoric Diester Hydrolases
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Polymerase Chain Reaction
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Pyrophosphatases / genetics
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Pyrophosphatases / metabolism
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RNA, Messenger / genetics
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RNA, Messenger / metabolism
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Receptors, Lysophosphatidic Acid / genetics*
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Receptors, Lysophosphatidic Acid / metabolism
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Reproducibility of Results
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Young Adult
Substances
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Multienzyme Complexes
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RNA, Messenger
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Receptors, Lysophosphatidic Acid
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Phosphoric Diester Hydrolases
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Phosphodiesterase I
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alkylglycerophosphoethanolamine phosphodiesterase
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Pyrophosphatases