Expression of Reactive Oxygen Species-Related Transcripts in Egyptian Children With Autism
The molecular basis of the pathophysiological role of oxidative stress in autism is understudied. Herein, we used polymerase chain reaction (PCR) array to analyze transcriptional pattern of 84 oxidative stress genes in peripheral blood mononuclear cell pools isolated from 32 autistic patients (16 mi...
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Published in | Biomarker Insights Vol. 2017; pp. 1 - 9-003 |
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Main Authors | , , , , , , , , |
Format | Journal Article |
Language | English |
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London, England
Libertas Academica
2017
SAGE Publications Sage Publications Ltd SAGE Publishing |
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Abstract | The molecular basis of the pathophysiological role of oxidative stress in autism is understudied. Herein, we used polymerase chain reaction (PCR) array to analyze transcriptional pattern of 84 oxidative stress genes in peripheral blood mononuclear cell pools isolated from 32 autistic patients (16 mild/moderate and 16 severe) and 16 healthy subjects (each sample is a pool from 4 autistic patients or 4 controls). The PCR array data were further validated by quantitative real-time PCR in 80 autistic children (55 mild/moderate and 25 severe) and 60 healthy subjects. Our data revealed downregulation in GCLM, SOD2, NCF2, PRNP, and PTGS2 transcripts (1.5, 3.8, 1.2, 1.7, and 2.2, respectively; P < .05 for all) in autistic group compared with controls. In addition, TXN and FTH1 exhibited 1.4- and 1.7-fold downregulation, respectively, in severe autistic patients when compared with mild/moderate group (P = .005 and .0008, respectively). This study helps in a better understanding of the underlying biology and related genetic factors of autism, and most importantly, it presents suggested candidate biomarkers for diagnosis and prognosis purposes as well as targets for therapeutic intervention. |
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AbstractList | The molecular basis of the pathophysiological role of oxidative stress in autism is understudied. Herein, we used polymerase chain reaction (PCR) array to analyze transcriptional pattern of 84 oxidative stress genes in peripheral blood mononuclear cell pools isolated from 32 autistic patients (16 mild/moderate and 16 severe) and 16 healthy subjects (each sample is a pool from 4 autistic patients or 4 controls). The PCR array data were further validated by quantitative real-time PCR in 80 autistic children (55 mild/moderate and 25 severe) and 60 healthy subjects. Our data revealed downregulation in GCLM, SOD2, NCF2, PRNP, and PTGS2 transcripts (1.5, 3.8, 1.2, 1.7, and 2.2, respectively; P < .05 for all) in autistic group compared with controls. In addition, TXN and FTH1 exhibited 1.4- and 1.7-fold downregulation, respectively, in severe autistic patients when compared with mild/moderate group (P = .005 and .0008, respectively). This study helps in a better understanding of the underlying biology and related genetic factors of autism, and most importantly, it presents suggested candidate biomarkers for diagnosis and prognosis purposes as well as targets for therapeutic intervention. The molecular basis of the pathophysiological role of oxidative stress in autism is understudied. Herein, we used polymerase chain reaction (PCR) array to analyze transcriptional pattern of 84 oxidative stress genes in peripheral blood mononuclear cell pools isolated from 32 autistic patients (16 mild/moderate and 16 severe) and 16 healthy subjects (each sample is a pool from 4 autistic patients or 4 controls). The PCR array data were further validated by quantitative real-time PCR in 80 autistic children (55 mild/moderate and 25 severe) and 60 healthy subjects. Our data revealed downregulation in GCLM, SOD2, NCF2, PRNP, and PTGS2 transcripts (1.5, 3.8, 1.2, 1.7, and 2.2, respectively;P < .05 for all) in autistic group compared with controls. In addition, TXN and FTH1 exhibited 1.4- and 1.7-fold downregulation, respectively, in severe autistic patients when compared with mild/moderate group (P = .005 and .0008, respectively). This study helps in a better understanding of the underlying biology and related genetic factors of autism, and most importantly, it presents suggested candidate biomarkers for diagnosis and prognosis purposes as well as targets for therapeutic intervention. The molecular basis of the pathophysiological role of oxidative stress in autism is understudied. Herein, we used polymerase chain reaction (PCR) array to analyze transcriptional pattern of 84 oxidative stress genes in peripheral blood mononuclear cell pools isolated from 32 autistic patients (16 mild/moderate and 16 severe) and 16 healthy subjects (each sample is a pool from 4 autistic patients or 4 controls). The PCR array data were further validated by quantitative real-time PCR in 80 autistic children (55 mild/moderate and 25 severe) and 60 healthy subjects. Our data revealed downregulation in GCLM, SOD2, NCF2, PRNP, and PTGS2 transcripts (1.5, 3.8, 1.2, 1.7, and 2.2, respectively; P < .05 for all) in autistic group compared with controls. In addition, TXN and FTH1 exhibited 1.4- and 1.7-fold downregulation, respectively, in severe autistic patients when compared with mild/moderate group (P = .005 and .0008, respectively). This study helps in a better understanding of the underlying biology and related genetic factors of autism, and most importantly, it presents suggested candidate biomarkers for diagnosis and prognosis purposes as well as targets for therapeutic intervention.The molecular basis of the pathophysiological role of oxidative stress in autism is understudied. Herein, we used polymerase chain reaction (PCR) array to analyze transcriptional pattern of 84 oxidative stress genes in peripheral blood mononuclear cell pools isolated from 32 autistic patients (16 mild/moderate and 16 severe) and 16 healthy subjects (each sample is a pool from 4 autistic patients or 4 controls). The PCR array data were further validated by quantitative real-time PCR in 80 autistic children (55 mild/moderate and 25 severe) and 60 healthy subjects. Our data revealed downregulation in GCLM, SOD2, NCF2, PRNP, and PTGS2 transcripts (1.5, 3.8, 1.2, 1.7, and 2.2, respectively; P < .05 for all) in autistic group compared with controls. In addition, TXN and FTH1 exhibited 1.4- and 1.7-fold downregulation, respectively, in severe autistic patients when compared with mild/moderate group (P = .005 and .0008, respectively). This study helps in a better understanding of the underlying biology and related genetic factors of autism, and most importantly, it presents suggested candidate biomarkers for diagnosis and prognosis purposes as well as targets for therapeutic intervention. The molecular basis of the pathophysiological role of oxidative stress in autism is understudied. Herein, we used polymerase chain reaction (PCR) array to analyze transcriptional pattern of 84 oxidative stress genes in peripheral blood mononuclear cell pools isolated from 32 autistic patients (16 mild/moderate and 16 severe) and 16 healthy subjects (each sample is a pool from 4 autistic patients or 4 controls). The PCR array data were further validated by quantitative real-time PCR in 80 autistic children (55 mild/moderate and 25 severe) and 60 healthy subjects. Our data revealed downregulation in , and transcripts (1.5, 3.8, 1.2, 1.7, and 2.2, respectively; < .05 for all) in autistic group compared with controls. In addition, and exhibited 1.4- and 1.7-fold downregulation, respectively, in severe autistic patients when compared with mild/moderate group ( = .005 and .0008, respectively). This study helps in a better understanding of the underlying biology and related genetic factors of autism, and most importantly, it presents suggested candidate biomarkers for diagnosis and prognosis purposes as well as targets for therapeutic intervention. The molecular basis of the pathophysiological role of oxidative stress in autism is understudied. Herein, we used polymerase chain reaction (PCR) array to analyze transcriptional pattern of 84 oxidative stress genes in peripheral blood mononuclear cell pools isolated from 32 autistic patients (16 mild/moderate and 16 severe) and 16 healthy subjects (each sample is a pool from 4 autistic patients or 4 controls). The PCR array data were further validated by quantitative real-time PCR in 80 autistic children (55 mild/moderate and 25 severe) and 60 healthy subjects. Our data revealed downregulation in GCLM, SOD2, NCF2, PRNP , and PTGS2 transcripts (1.5, 3.8, 1.2, 1.7, and 2.2, respectively; P < .05 for all) in autistic group compared with controls. In addition, TXN and FTH1 exhibited 1.4- and 1.7-fold downregulation, respectively, in severe autistic patients when compared with mild/moderate group ( P = .005 and .0008, respectively). This study helps in a better understanding of the underlying biology and related genetic factors of autism, and most importantly, it presents suggested candidate biomarkers for diagnosis and prognosis purposes as well as targets for therapeutic intervention. |
Author | Magda F Mohamed Reham M Dawood Marwa K Ibrahim Noha G Bader El Din Mostafa K El Awady Maha Hemimi Tawfeek H Abdelhafez Nagwa A Meguid Said A S Ghozlan |
AuthorAffiliation | 1 Department of Research on Children with Special Needs, Medical Research Division, National Research Centre, Giza, Egypt 4 Microbial Biotechnology Department, Genetic Engineering Division, National Research Centre, Giza, Egypt 3 Department of Chemistry (Biochemistry Branch), Faculty of Science, Cairo University, Giza, Egypt 2 Department of Chemistry, Faculty of Science, Cairo University, Giza, Egypt |
AuthorAffiliation_xml | – name: 2 Department of Chemistry, Faculty of Science, Cairo University, Giza, Egypt – name: 4 Microbial Biotechnology Department, Genetic Engineering Division, National Research Centre, Giza, Egypt – name: 3 Department of Chemistry (Biochemistry Branch), Faculty of Science, Cairo University, Giza, Egypt – name: 1 Department of Research on Children with Special Needs, Medical Research Division, National Research Centre, Giza, Egypt |
Author_xml | – sequence: 1 givenname: Nagwa A surname: Meguid fullname: Meguid, Nagwa A – sequence: 2 givenname: Said A S surname: Ghozlan fullname: Ghozlan, Said A S – sequence: 3 givenname: Magda F surname: Mohamed fullname: Mohamed, Magda F – sequence: 4 givenname: Marwa K surname: Ibrahim fullname: Ibrahim, Marwa K – sequence: 5 givenname: Reham M surname: Dawood fullname: Dawood, Reham M – sequence: 6 givenname: Noha G surname: Bader El Din fullname: Bader El Din, Noha G – sequence: 7 givenname: Tawfeek H surname: Abdelhafez fullname: Abdelhafez, Tawfeek H – sequence: 8 givenname: Maha surname: Hemimi fullname: Hemimi, Maha – sequence: 9 givenname: Mostafa K surname: El Awady fullname: El Awady, Mostafa K |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/28469396$$D View this record in MEDLINE/PubMed |
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Keywords | Autism neurodevelopmental disorders gene expression oxidative stress ROS PCR array |
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Snippet | The molecular basis of the pathophysiological role of oxidative stress in autism is understudied. Herein, we used polymerase chain reaction (PCR) array to... |
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SubjectTerms | Amino acids Antioxidants Authorship Autism Biomarkers Children Children & youth Diagnostic tests Enzymes Experiments Families & family life Gene expression Genetic factors Medical research Medical screening Original Research Oxidative stress Peer review Peripheral blood Polymerase chain reaction Proteins Reactive oxygen species Studies Superoxide dismutase Transcription |
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Title | Expression of Reactive Oxygen Species-Related Transcripts in Egyptian Children With Autism |
URI | https://www.airitilibrary.com/Article/Detail/P20160527001-201712-201808280019-201808280019-1-9-003 https://journals.sagepub.com/doi/full/10.1177/1177271917691035 https://www.ncbi.nlm.nih.gov/pubmed/28469396 https://www.proquest.com/docview/2081551121 https://www.proquest.com/docview/2425620835 https://www.proquest.com/docview/1895273829 https://pubmed.ncbi.nlm.nih.gov/PMC5391985 https://doaj.org/article/7bbf01a0f6754f45b40be70962535b27 |
Volume | 2017 |
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