title: Nogo A, B and C expression in schizophrenia, depression and bipolar frontal cortex, and correlation of Nogo expression with CAA/TATC polymorphism in 3'-UTR.
abstract: Schizophrenia may result from altered gene expression leading to abnormal neurodevelopment. In a search for genes with altered expression in schizophrenia, our previous work on human frontal cerebral cortex found the mRNA of Nogo, a myelin-associated protein which inhibits the outgrowth of neurites and nerve terminals, to be overexpressed in schizophrenia. Because those earlier results did not examine tissues for the separate Nogo A, B and C isoforms from age- and sex-matched individuals, we repeated the study for all three isoforms, using a new set of tissues from matched individuals, and using the more accurate method of quantitative real-time PCR (polymerase chain reaction). We found Nogo C to be overexpressed by 26% in the schizophrenia tissues, which is in accordance with our earlier results. The expression of Nogo B was statistically significantly reduced by 17% in the frontal cortices from individuals who had been diagnosed as having had severe depression. Furthermore, we show that there is a direct correlation between the expression of Nogo A and C and the presence of alleles with a CAA insert, irrespective of disease status. While upregulation of Nogo C expression may play a role in schizophrenia, altered Nogo B may contribute to the clinical condition of depression. Nogo A showed a statistically non-significant increase in expression in schizophrenia.
authors.affiliation: Department of Pharmacology, Medical Sciences Building 4344, University of Toronto, 1 King's College Circle, Toronto, Canada M5S 1A8.
authors.forename: Gabriela
authors.initials: G
authors.lastname: Novak
authors.forename: Teresa
authors.initials: T
authors.lastname: Tallerico
mesh_terms: D020413:3' Untranslated Regions; D000328:Adult; D001714:Bipolar Disorder / Q000235:genetics / Q000473:pathology / Q000503:physiopathology; D018076:DNA, Complementary; D003863:Depression / Q000235:genetics / Q000473:pathology / Q000503:physiopathology; D005260:Female; D005625:Frontal Lobe / Q000378:metabolism*; D015870:Gene Expression / Q000502:physiology; D005787:Gene Frequency; D020022:Genetic Predisposition to Disease; D006801:Humans; D008297:Male; D008875:Middle Aged; D009185:Myelin Proteins / Q000235:genetics / Q000378:metabolism*; D000070798:Nogo Proteins; D011110:Polymorphism, Genetic / Q000235:genetics*; D011180:Postmortem Changes; D020033:Protein Isoforms; D012333:RNA, Messenger / Q000378:metabolism; D020133:Reverse Transcriptase Polymerase Chain Reaction / Q000379:methods; D012559:Schizophrenia / Q000235:genetics / Q000473:pathology / Q000503:physiopathology
chemical_list: D020413:3' Untranslated Regions; D018076:DNA, Complementary; D009185:Myelin Proteins; D000070798:Nogo Proteins; D020033:Protein Isoforms; D012333:RNA, Messenger; C000603199:RTN4 protein, human