Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:Q9UIJ5 (Rec)
 58,342 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Onset of motoneuron death characterizing amyotrophic lateral sclerosis (ALS) is closely linked to modified astrocytic and glial environments. Here, we show that in the spinal cord from transgenic rat overexpressing mutated human SOD1, aquaporin-4 mRNA and protein are specifically overexpressed in the gray matter at end stage of disease. Immunohistochemistry and double immunofluorescence allowed to detect, in the spinal cord gray matter of the ALS rat, increased aquaporin-4 surrounding both vessel and motoneuron perikarya. The use of pre-embedding immunohistochemistry at electron microscopic level confirmed such localization associated with swollen astrocytic processes surrounding the vessels. The AQP4 immunohistochemical labeling surrounding several motoneuron perikarya was only seen in ALS rats. Identification of this AQP4-positive cellular type remains unclear.
Anat Rec (Hoboken) 2009 Feb
PMID:Aquaporin-4 overexpression in rat ALS model. 1908 2

Aquaporin 4(AQP4) is a water channel protein strongly expressed in the central nervous system in perimicrovessel astrocyte foot processes, the glia limitans, and ependyma. Expression of AQP4 is highest at the blood-brain barrier and blood-spinal cord barrier, supporting its critical function in material transport across these structures. Recently, presence of the anti-aquaporin-4 antibody in sera has been used as an important diagnostic tool for neuromyelitis optica, suggesting a potential role in central nervous system inflammation. The aim of the present study was to examine AQP4 protein expression in the cerebellum and spinal cord from rats with experimental autoimmune encephalomyelitis. By western blot analysis, AQP4 expression increased during experimental autoimmune encephalomyelitis development, and peaked at onset (lumbar enlargement) or climax (cerebellum) of neurological signs of experimental autoimmune encephalomyelitis. There was also a faster and more pronounced increase in permeability in the cerebellar blood-brain barrier and the lumbar enlargement blood-spinal cord barrier consistent with AQP4 expression, which was manifested by increased Evans Blue leakage and reduced tight junction protein expression. In conclusion, aquaporin upregulation may be involved in the development of inflammation in the acute phase of experimental autoimmune encephalomyelitis, and may correlate with damage to central nervous system barrier function.
Anat Rec (Hoboken) 2011 Jan
PMID:The relationship between aquaporin-4 expression and blood-brain and spinal cord barrier permeability following experimental autoimmune encephalomyelitis in the rat. 2115 15