Mitochondrial-related gene expression changes are sensitive to agonal-pH state: implications for brain disorders
Mitochondrial defects in gene expression have been implicated in the pathophysiology of bipolar disorder and schizophrenia. We have now contrasted control brains with low pH versus high pH and showed that 28% of genes in mitochondrial-related pathways meet criteria for differential expression. A maj...
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| Published in | Molecular psychiatry Vol. 11; no. 7; pp. 663 - 679 |
|---|---|
| Main Authors | , , , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
London
Nature Publishing Group UK
01.07.2006
Nature Publishing Group |
| Subjects | |
| Online Access | Get full text |
| ISSN | 1359-4184 1476-5578 |
| DOI | 10.1038/sj.mp.4001830 |
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| Abstract | Mitochondrial defects in gene expression have been implicated in the pathophysiology of bipolar disorder and schizophrenia. We have now contrasted control brains with low pH versus high pH and showed that 28% of genes in mitochondrial-related pathways meet criteria for differential expression. A majority of genes in the mitochondrial, chaperone and proteasome pathways of nuclear DNA-encoded gene expression were decreased with decreased brain pH, whereas a majority of genes in the apoptotic and reactive oxygen stress pathways showed an increased gene expression with a decreased brain pH. There was a significant increase in mitochondrial DNA copy number and mitochondrial DNA gene expression with increased agonal duration. To minimize effects of agonal-pH state on mood disorder comparisons, two classic approaches were used, removing all subjects with low pH and agonal factors from analysis, or grouping low and high pH as a separate variable. Three groups of potential candidate genes emerged that may be mood disorder related: (a) genes that showed no sensitivity to pH but were differentially expressed in bipolar disorder or major depressive disorder; (b) genes that were altered by agonal-pH in one direction but altered in mood disorder in the opposite direction to agonal-pH and (c) genes with agonal-pH sensitivity that displayed the same direction of changes in mood disorder. Genes from these categories such as NR4A1 and HSPA2 were confirmed with Q-PCR. The interpretation of postmortem brain studies involving broad mitochondrial gene expression and related pathway alterations must be monitored against the strong effect of agonal-pH state. Genes with the least sensitivity to agonal-pH could present a starting point for candidate gene search in neuropsychiatric disorders. |
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| AbstractList | Mitochondrial defects in gene expression have been implicated in the pathophysiology of bipolar disorder and schizophrenia. We have now contrasted control brains with low pH versus high pH and showed that 28% of genes in mitochondrial-related pathways meet criteria for differential expression. A majority of genes in the mitochondrial, chaperone and proteasome pathways of nuclear DNA-encoded gene expression were decreased with decreased brain pH, whereas a majority of genes in the apoptotic and reactive oxygen stress pathways showed an increased gene expression with a decreased brain pH. There was a significant increase in mitochondrial DNA copy number and mitochondrial DNA gene expression with increased agonal duration. To minimize effects of agonal-pH state on mood disorder comparisons, two classic approaches were used, removing all subjects with low pH and agonal factors from analysis, or grouping low and high pH as a separate variable. Three groups of potential candidate genes emerged that may be mood disorder related: (a) genes that showed no sensitivity to pH but were differentially expressed in bipolar disorder or major depressive disorder; (b) genes that were altered by agonal-pH in one direction but altered in mood disorder in the opposite direction to agonal-pH and (c) genes with agonal-pH sensitivity that displayed the same direction of changes in mood disorder. Genes from these categories such as NR4A1 and HSPA2 were confirmed with Q-PCR. The interpretation of postmortem brain studies involving broad mitochondrial gene expression and related pathway alterations must be monitored against the strong effect of agonal-pH state. Genes with the least sensitivity to agonal-pH could present a starting point for candidate gene search in neuropsychiatric disorders. Mitochondrial defects in gene expression have been implicated in the pathophysiology of bipolar disorder and schizophrenia. We have now contrasted control brains with low pH versus high pH and showed that 28% of genes in mitochondrial-related pathways meet criteria for differential expression. A majority of genes in the mitochondrial, chaperone and proteasome pathways of nuclear DNA-encoded gene expression were decreased with decreased brain pH, whereas a majority of genes in the apoptotic and reactive oxygen stress pathways showed an increased gene expression with a decreased brain pH. There was a significant increase in mitochondrial DNA copy number and mitochondrial DNA gene expression with increased agonal duration. To minimize effects of agonal-pH state on mood disorder comparisons, two classic approaches were used, removing all subjects with low pH and agonal factors from analysis, or grouping low and high pH as a separate variable. Three groups of potential candidate genes emerged that may be mood disorder related: (a) genes that showed no sensitivity to pH but were differentially expressed in bipolar disorder or major depressive disorder; (b) genes that were altered by agonal-pH in one direction but altered in mood disorder in the opposite direction to agonal-pH and (c) genes with agonal-pH sensitivity that displayed the same direction of changes in mood disorder. Genes from these categories such as NR4A1 and HSPA2 were confirmed with Q-PCR. The interpretation of postmortem brain studies involving broad mitochondrial gene expression and related pathway alterations must be monitored against the strong effect of agonal-pH state. Genes with the least sensitivity to agonal-pH could present a starting point for candidate gene search in neuropsychiatric disorders.Molecular Psychiatry (2006) 11, 663-679. doi:10.1038/sj.mp.4001830; published online 25 April 2006 Mitochondrial defects in gene expression have been implicated in the pathophysiology of bipolar disorder and schizophrenia. We have now contrasted control brains with low pH versus high pH and showed that 28% of genes in mitochondrial-related pathways meet criteria for differential expression. A majority of genes in the mitochondrial, chaperone and proteasome pathways of nuclear DNA-encoded gene expression were decreased with decreased brain pH, whereas a majority of genes in the apoptotic and reactive oxygen stress pathways showed an increased gene expression with a decreased brain pH. There was a significant increase in mitochondrial DNA copy number and mitochondrial DNA gene expression with increased agonal duration. To minimize effects of agonal-pH state on mood disorder comparisons, two classic approaches were used, removing all subjects with low pH and agonal factors from analysis, or grouping low and high pH as a separate variable. Three groups of potential candidate genes emerged that may be mood disorder related: (a) genes that showed no sensitivity to pH but were differentially expressed in bipolar disorder or major depressive disorder; (b) genes that were altered by agonal-pH in one direction but altered in mood disorder in the opposite direction to agonal-pH and (c) genes with agonal-pH sensitivity that displayed the same direction of changes in mood disorder. Genes from these categories such as NR4A1 and HSPA2 were confirmed with Q-PCR. The interpretation of postmortem brain studies involving broad mitochondrial gene expression and related pathway alterations must be monitored against the strong effect of agonal-pH state. Genes with the least sensitivity to agonal-pH could present a starting point for candidate gene search in neuropsychiatric disorders.Mitochondrial defects in gene expression have been implicated in the pathophysiology of bipolar disorder and schizophrenia. We have now contrasted control brains with low pH versus high pH and showed that 28% of genes in mitochondrial-related pathways meet criteria for differential expression. A majority of genes in the mitochondrial, chaperone and proteasome pathways of nuclear DNA-encoded gene expression were decreased with decreased brain pH, whereas a majority of genes in the apoptotic and reactive oxygen stress pathways showed an increased gene expression with a decreased brain pH. There was a significant increase in mitochondrial DNA copy number and mitochondrial DNA gene expression with increased agonal duration. To minimize effects of agonal-pH state on mood disorder comparisons, two classic approaches were used, removing all subjects with low pH and agonal factors from analysis, or grouping low and high pH as a separate variable. Three groups of potential candidate genes emerged that may be mood disorder related: (a) genes that showed no sensitivity to pH but were differentially expressed in bipolar disorder or major depressive disorder; (b) genes that were altered by agonal-pH in one direction but altered in mood disorder in the opposite direction to agonal-pH and (c) genes with agonal-pH sensitivity that displayed the same direction of changes in mood disorder. Genes from these categories such as NR4A1 and HSPA2 were confirmed with Q-PCR. The interpretation of postmortem brain studies involving broad mitochondrial gene expression and related pathway alterations must be monitored against the strong effect of agonal-pH state. Genes with the least sensitivity to agonal-pH could present a starting point for candidate gene search in neuropsychiatric disorders. |
| Audience | Academic |
| Author | Akil, H Walsh, D M Neal, C Myers, R Li, J Tomita, H Burmeister, M Speed, T Vawter, M P Shao, L Evans, S Choudary, P Bolstad, B Meng, F Atz, M Jones, E G Bunney, W E Watson, S J |
| AuthorAffiliation | 3 Biostatistics, University of California, Berkeley, CA, USA 2 Mental Health Research Institute, University of Michigan, Ann Arbor, MI, USA 1 Department of Psychiatry, University of California, Irvine, CA, USA 4 Stanford Human Genome Center, Stanford University, Palo Alto, CA, USA 6 University of Hawaii, John A. Burns School of Medicine, Honolulu, HI, USA 5 Center for Neuroscience, University of California, Davis, CA, USA |
| AuthorAffiliation_xml | – name: 2 Mental Health Research Institute, University of Michigan, Ann Arbor, MI, USA – name: 3 Biostatistics, University of California, Berkeley, CA, USA – name: 1 Department of Psychiatry, University of California, Irvine, CA, USA – name: 4 Stanford Human Genome Center, Stanford University, Palo Alto, CA, USA – name: 5 Center for Neuroscience, University of California, Davis, CA, USA – name: 6 University of Hawaii, John A. Burns School of Medicine, Honolulu, HI, USA |
| Author_xml | – sequence: 1 givenname: M P surname: Vawter fullname: Vawter, M P email: mvawter@uci.edu organization: Department of Psychiatry, University of California – sequence: 2 givenname: H surname: Tomita fullname: Tomita, H organization: Department of Psychiatry, University of California – sequence: 3 givenname: F surname: Meng fullname: Meng, F organization: Mental Health Research Institute, University of Michigan – sequence: 4 givenname: B surname: Bolstad fullname: Bolstad, B organization: Biostatistics, University of California – sequence: 5 givenname: J surname: Li fullname: Li, J organization: Stanford Human Genome Center, Stanford University – sequence: 6 givenname: S surname: Evans fullname: Evans, S organization: Mental Health Research Institute, University of Michigan – sequence: 7 givenname: P surname: Choudary fullname: Choudary, P organization: Center for Neuroscience, University of California – sequence: 8 givenname: M surname: Atz fullname: Atz, M organization: Department of Psychiatry, University of California – sequence: 9 givenname: L surname: Shao fullname: Shao, L organization: Department of Psychiatry, University of California – sequence: 10 givenname: C surname: Neal fullname: Neal, C organization: University of Hawaii, John A. Burns School of Medicine – sequence: 11 givenname: D M surname: Walsh fullname: Walsh, D M organization: Department of Psychiatry, University of California – sequence: 12 givenname: M surname: Burmeister fullname: Burmeister, M organization: Mental Health Research Institute, University of Michigan – sequence: 13 givenname: T surname: Speed fullname: Speed, T organization: Biostatistics, University of California – sequence: 14 givenname: R surname: Myers fullname: Myers, R organization: Stanford Human Genome Center, Stanford University – sequence: 15 givenname: E G surname: Jones fullname: Jones, E G organization: Center for Neuroscience, University of California – sequence: 16 givenname: S J surname: Watson fullname: Watson, S J organization: Mental Health Research Institute, University of Michigan – sequence: 17 givenname: H surname: Akil fullname: Akil, H organization: Mental Health Research Institute, University of Michigan – sequence: 18 givenname: W E surname: Bunney fullname: Bunney, W E organization: Department of Psychiatry, University of California |
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| Copyright | Springer Nature Limited 2006 2006 INIST-CNRS COPYRIGHT 2006 Nature Publishing Group Copyright Nature Publishing Group Jul 2006 Nature Publishing Group 2006. 2006 Nature Publishing Group All rights reserved 2006 |
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| Issue | 7 |
| Keywords | proteasome apoptosis recurrent major depressive disorder chaperone bipolar disorder I mitochondria Mood disorder Human Multicatalytic endopeptidase complex Relapse Enzyme Central nervous system Depression Bipolar disorder Gene expression Encephalon Peptidases Mitochondria pH Hydrolases Apoptosis |
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| Snippet | Mitochondrial defects in gene expression have been implicated in the pathophysiology of bipolar disorder and schizophrenia. We have now contrasted control... |
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| SubjectTerms | Adult and adolescent clinical studies Antidepressive Agents - pharmacology Apoptosis Apoptosis - genetics Behavioral Sciences Biological and medical sciences Biological Psychology Bipolar disorder Bipolar Disorder - drug therapy Bipolar Disorder - genetics Bipolar Disorder - metabolism Bipolar Disorder - pathology Bipolar disorders Brain Brain - drug effects Brain - metabolism Brain - pathology Cerebellum - drug effects Cerebellum - metabolism Cerebellum - pathology Copy number Death Depression Depressive Disorder - genetics Depressive Disorder - metabolism Depressive Disorder - pathology DNA, Mitochondrial - genetics DNA, Mitochondrial - metabolism Emotional disorders Female Gene Dosage Gene expression Gene Expression Regulation - drug effects Gene Expression Regulation - physiology Gyrus Cinguli - drug effects Gyrus Cinguli - metabolism Gyrus Cinguli - pathology Humans Hydrogen-Ion Concentration In Situ Hybridization Lithium - pharmacology Male Medical sciences Medicine Medicine & Public Health Mental disorders Middle Aged Mitochondria - drug effects Mitochondria - metabolism Mitochondrial DNA Molecular Chaperones - biosynthesis Molecular Chaperones - genetics Mood Mood disorders Neoplasm Proteins - biosynthesis Neoplasm Proteins - genetics Nerve Tissue Proteins - biosynthesis Nerve Tissue Proteins - genetics Neurosciences Oligonucleotide Array Sequence Analysis original-article Oxidative Stress - genetics pH effects Pharmacotherapy Polymerase Chain Reaction Postmortem Changes Prefrontal Cortex - drug effects Prefrontal Cortex - metabolism Prefrontal Cortex - pathology Proteasome Endopeptidase Complex - metabolism Proteasomes Psychiatry Psychology. Psychoanalysis. Psychiatry Psychopathology. Psychiatry RNA, Messenger - biosynthesis RNA, Messenger - genetics Schizophrenia Selective Serotonin Reuptake Inhibitors - pharmacology Time Factors |
| Title | Mitochondrial-related gene expression changes are sensitive to agonal-pH state: implications for brain disorders |
| URI | https://link.springer.com/article/10.1038/sj.mp.4001830 https://www.ncbi.nlm.nih.gov/pubmed/16636682 https://www.proquest.com/docview/221254851 https://www.proquest.com/docview/2645752187 https://www.proquest.com/docview/68579896 https://www.proquest.com/docview/759318577 https://pubmed.ncbi.nlm.nih.gov/PMC3098558 |
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