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DNA Methylation and Gene Expression of Matrix Metalloproteinase 9 Gene in Deficit and Non-deficit Schizophrenia

The biological pathology of deficit schizophrenia (DS) remains unclear. Matrix metalloproteinase 9 (MMP9) might be associated with neural plasticity and glutamate regulation, involved in schizophrenia pathogenesis. This study explores gene expression and DNA methylation of MMP9 in peripheral blood m...

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Autores principales: Gao, Ju, Yi, Hongwei, Tang, Xiaowei, Feng, Xiaotang, Yu, Miao, Sha, Weiwei, Wang, Xiang, Zhang, Xiaobin, Zhang, Xiangrong
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6297256/
https://www.ncbi.nlm.nih.gov/pubmed/30619470
http://dx.doi.org/10.3389/fgene.2018.00646
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author Gao, Ju
Yi, Hongwei
Tang, Xiaowei
Feng, Xiaotang
Yu, Miao
Sha, Weiwei
Wang, Xiang
Zhang, Xiaobin
Zhang, Xiangrong
author_facet Gao, Ju
Yi, Hongwei
Tang, Xiaowei
Feng, Xiaotang
Yu, Miao
Sha, Weiwei
Wang, Xiang
Zhang, Xiaobin
Zhang, Xiangrong
author_sort Gao, Ju
collection PubMed
description The biological pathology of deficit schizophrenia (DS) remains unclear. Matrix metalloproteinase 9 (MMP9) might be associated with neural plasticity and glutamate regulation, involved in schizophrenia pathogenesis. This study explores gene expression and DNA methylation of MMP9 in peripheral blood mononuclear cells (PBMCs) and their relationship with clinical symptoms in DS and non-deficit schizophrenia (NDS). Pyrosequencing was used to determine DNA methylation at CpG sites in exon 4 and exon 5 of MMP9 in 51 DS patients, 53 NDS patients and 50 healthy subjects (HC). RT-qPCR was used to detect MMP9 expression. Clinical symptoms were assessed by BPRS, SANS and SAPS scales. MMP9 expression in PBMCs was significantly higher in DS than NDS and HC subjects. Compared to NDS patients, DS patients had significantly lower DNA methylation at individual CpG sites in exon 4 and exon 5 of MMP9. Correlation analysis showed that DNA methylation in exon 4 was negatively correlated with gene expression in DS group. Positive correlation was found between MMP9 expression and negative symptoms in total schizophrenic patients. The social amotivation factor of SANS and negative syndrome of BPRS was negatively correlated with DNA methylation of CpG5-1 in DS patients but not in NDS patients. DS patients showed a specific abnormality of peripheral MMP9 expression and DNA methylation, indicating a pathological mechanism underlying DS as a specific subgroup of schizophrenia.
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spelling pubmed-62972562019-01-07 DNA Methylation and Gene Expression of Matrix Metalloproteinase 9 Gene in Deficit and Non-deficit Schizophrenia Gao, Ju Yi, Hongwei Tang, Xiaowei Feng, Xiaotang Yu, Miao Sha, Weiwei Wang, Xiang Zhang, Xiaobin Zhang, Xiangrong Front Genet Genetics The biological pathology of deficit schizophrenia (DS) remains unclear. Matrix metalloproteinase 9 (MMP9) might be associated with neural plasticity and glutamate regulation, involved in schizophrenia pathogenesis. This study explores gene expression and DNA methylation of MMP9 in peripheral blood mononuclear cells (PBMCs) and their relationship with clinical symptoms in DS and non-deficit schizophrenia (NDS). Pyrosequencing was used to determine DNA methylation at CpG sites in exon 4 and exon 5 of MMP9 in 51 DS patients, 53 NDS patients and 50 healthy subjects (HC). RT-qPCR was used to detect MMP9 expression. Clinical symptoms were assessed by BPRS, SANS and SAPS scales. MMP9 expression in PBMCs was significantly higher in DS than NDS and HC subjects. Compared to NDS patients, DS patients had significantly lower DNA methylation at individual CpG sites in exon 4 and exon 5 of MMP9. Correlation analysis showed that DNA methylation in exon 4 was negatively correlated with gene expression in DS group. Positive correlation was found between MMP9 expression and negative symptoms in total schizophrenic patients. The social amotivation factor of SANS and negative syndrome of BPRS was negatively correlated with DNA methylation of CpG5-1 in DS patients but not in NDS patients. DS patients showed a specific abnormality of peripheral MMP9 expression and DNA methylation, indicating a pathological mechanism underlying DS as a specific subgroup of schizophrenia. Frontiers Media S.A. 2018-12-11 /pmc/articles/PMC6297256/ /pubmed/30619470 http://dx.doi.org/10.3389/fgene.2018.00646 Text en Copyright © 2018 Gao, Yi, Tang, Feng, Yu, Sha, Wang, Zhang and Zhang. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Genetics
Gao, Ju
Yi, Hongwei
Tang, Xiaowei
Feng, Xiaotang
Yu, Miao
Sha, Weiwei
Wang, Xiang
Zhang, Xiaobin
Zhang, Xiangrong
DNA Methylation and Gene Expression of Matrix Metalloproteinase 9 Gene in Deficit and Non-deficit Schizophrenia
title DNA Methylation and Gene Expression of Matrix Metalloproteinase 9 Gene in Deficit and Non-deficit Schizophrenia
title_full DNA Methylation and Gene Expression of Matrix Metalloproteinase 9 Gene in Deficit and Non-deficit Schizophrenia
title_fullStr DNA Methylation and Gene Expression of Matrix Metalloproteinase 9 Gene in Deficit and Non-deficit Schizophrenia
title_full_unstemmed DNA Methylation and Gene Expression of Matrix Metalloproteinase 9 Gene in Deficit and Non-deficit Schizophrenia
title_short DNA Methylation and Gene Expression of Matrix Metalloproteinase 9 Gene in Deficit and Non-deficit Schizophrenia
title_sort dna methylation and gene expression of matrix metalloproteinase 9 gene in deficit and non-deficit schizophrenia
topic Genetics
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6297256/
https://www.ncbi.nlm.nih.gov/pubmed/30619470
http://dx.doi.org/10.3389/fgene.2018.00646
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