Sp1 Expression Is Disrupted in Schizophrenia; A Possible Mechanism for the Abnormal Expression of Mitochondrial Complex I Genes, NDUFV1 and NDUFV2 英文参考文献.docVIP

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Sp1 Expression Is Disrupted in Schizophrenia; A Possible Mechanism for the Abnormal Expression of Mitochondrial Complex I Genes, NDUFV1 and NDUFV2 英文参考文献.doc

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Sp1 Expression Is Disrupted in Schizophrenia; A Possible Mechanism for the Abnormal Expression of Mitochondrial Complex I Genes, NDUFV1 and NDUFV2 英文参考文献

Sp1ExpressionIsDisruptedinSchizophrenia;APossible MechanismfortheAbnormalExpressionof MitochondrialComplexIGenes,NDUFV1andNDUFV2 DoritBen-Shachar1,2*,RachelKarry1,2 1LaboratoryofPsychobiology,DepartmentofPsychiatry,RambamMedicalCenter,RuthandBruceRappaportFacultyofMedicine,TechnionIsrael InstituteofTechnology,Haifa,Israel,2LaboratoryofMolecularMedicine,RambamMedicalCenter,RuthandBruceRappaportFacultyofMedicine, TechnionIsraelInstituteofTechnology,Haifa,Israel Background.Theprevailinghypothesisregardsschizophreniaasapolygenicdisease,inwhichmultiplegenescombinewith each other and with environmental stimuli to produce the variance of its clinical symptoms. We investigated whether the ubiquitoustranscriptionfactorSp1isabnormallyexpressedinschizophrenia,andconsequentlycanaffecttheexpressionof genesimplicatedinthisdisorder.Methodology/PrincipalFindings.mRNAofSp1andofmitochondrialcomplexIsubunits (NDUFV1,NDUFV2)wasanalyzedinthreepostmortembrainregionsobtainedfromtheStanleyFoundationBrainCollection, andinlymphocytesofschizophrenicpatientsandcontrols.Sp1roleinthetranscriptionofthesegeneswasstudiedaswell.Sp1 wasabnormallyexpressedinschizophreniainbothbrainandperiphery.ItsmRNAalterationpatternparalleledthatofNDUFV1 and NDUFV2, decreasing in the prefrontal cortex and the striatum, while increasing in the parieto-occipital cortex and in lymphocytesofschizophrenicpatientsascomparedwithcontrols.Moreover,ahighandsignificantcorrelationbetweenthese genes existed in normal subjects, but was distorted in patients. Sp1 role in the regulation of complex I subunits, was demonstrated by the ability of the Sp1/DNA binding inhibitor, mithramycin, to inhibit the transcription of NDUFV1 and NDUFV2,inneuroblastomacells.Inaddition,Sp1activatedNDUFV2promoterbybindingtoitsthreeGC-boxes.Bothactivation and binding were inhibited by mithramycin. Conclusions/Significance. These findings suggest that abnormality in Sp1, which can be the main activator/repressor or act in combination with additional t