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Differential gene expression profiles between two subtypes of ischemic stroke with blood stasis syndromes

Ischemic stroke is a cerebrovascular thrombotic disease with high morbidity and mortality. Qi deficiency blood stasis (QDBS) and Yin deficiency blood stasis (YDBS) are the two major subtypes of ischemic stroke according to the theories of traditional Chinese medicine. This study was conducted to dis...

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Autores principales: Liu, Tian-Long, Liu, Min-Na, Xu, Xin-Liang, Liu, Wen-Xing, Shang, Pei-Jin, Zhai, Xiao-Hu, Xu, Hang, Ding, Yi, Li, Yu-Wen, Wen, Ai-Dong
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Impact Journals LLC 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5762346/
https://www.ncbi.nlm.nih.gov/pubmed/29340078
http://dx.doi.org/10.18632/oncotarget.22877
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author Liu, Tian-Long
Liu, Min-Na
Xu, Xin-Liang
Liu, Wen-Xing
Shang, Pei-Jin
Zhai, Xiao-Hu
Xu, Hang
Ding, Yi
Li, Yu-Wen
Wen, Ai-Dong
author_facet Liu, Tian-Long
Liu, Min-Na
Xu, Xin-Liang
Liu, Wen-Xing
Shang, Pei-Jin
Zhai, Xiao-Hu
Xu, Hang
Ding, Yi
Li, Yu-Wen
Wen, Ai-Dong
author_sort Liu, Tian-Long
collection PubMed
description Ischemic stroke is a cerebrovascular thrombotic disease with high morbidity and mortality. Qi deficiency blood stasis (QDBS) and Yin deficiency blood stasis (YDBS) are the two major subtypes of ischemic stroke according to the theories of traditional Chinese medicine. This study was conducted to distinguish these two syndromes at transcriptomics level and explore the underlying mechanisms. Male rats were randomly divided into three groups: sham group, QDBS/MCAO group and YDBS/MCAO group. Morphological changes were assessed after 24 h of reperfusion. Microarray analysis with circulating mRNA was then performed to identify differential gene expression profile, gene ontology and pathway enrichment analyses were carried out to predict the gene function, gene co-expression and pathway networks were constructed to identify the hub biomarkers, which were further validated by western blotting and Tunel staining analysis. Three subsets of dysregulated genes were acquired, including 445 QDBS-specific genes, 490 YDBS-specific genes and 1676 blood stasis common genes. Our work reveals for the first time that T cell receptor, MAPK and apoptosis pathway were identified as the hub pathways based on the pathway networks, while Nfκb1, Egfr and Casp3 were recognized as the hub genes by co-expression networks. This research helps contribute to a clearer understanding of the pathological characteristics of ischemic stroke with QDBS and YDBS syndrome, the proposed biomarkers might provide insight into the accurate diagnose and proper treatment for ischemic stroke with blood stasis syndrome.
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spelling pubmed-57623462018-01-16 Differential gene expression profiles between two subtypes of ischemic stroke with blood stasis syndromes Liu, Tian-Long Liu, Min-Na Xu, Xin-Liang Liu, Wen-Xing Shang, Pei-Jin Zhai, Xiao-Hu Xu, Hang Ding, Yi Li, Yu-Wen Wen, Ai-Dong Oncotarget Research Paper Ischemic stroke is a cerebrovascular thrombotic disease with high morbidity and mortality. Qi deficiency blood stasis (QDBS) and Yin deficiency blood stasis (YDBS) are the two major subtypes of ischemic stroke according to the theories of traditional Chinese medicine. This study was conducted to distinguish these two syndromes at transcriptomics level and explore the underlying mechanisms. Male rats were randomly divided into three groups: sham group, QDBS/MCAO group and YDBS/MCAO group. Morphological changes were assessed after 24 h of reperfusion. Microarray analysis with circulating mRNA was then performed to identify differential gene expression profile, gene ontology and pathway enrichment analyses were carried out to predict the gene function, gene co-expression and pathway networks were constructed to identify the hub biomarkers, which were further validated by western blotting and Tunel staining analysis. Three subsets of dysregulated genes were acquired, including 445 QDBS-specific genes, 490 YDBS-specific genes and 1676 blood stasis common genes. Our work reveals for the first time that T cell receptor, MAPK and apoptosis pathway were identified as the hub pathways based on the pathway networks, while Nfκb1, Egfr and Casp3 were recognized as the hub genes by co-expression networks. This research helps contribute to a clearer understanding of the pathological characteristics of ischemic stroke with QDBS and YDBS syndrome, the proposed biomarkers might provide insight into the accurate diagnose and proper treatment for ischemic stroke with blood stasis syndrome. Impact Journals LLC 2017-12-04 /pmc/articles/PMC5762346/ /pubmed/29340078 http://dx.doi.org/10.18632/oncotarget.22877 Text en Copyright: © 2017 Liu et al. http://creativecommons.org/licenses/by/3.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/3.0/) 3.0 (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
spellingShingle Research Paper
Liu, Tian-Long
Liu, Min-Na
Xu, Xin-Liang
Liu, Wen-Xing
Shang, Pei-Jin
Zhai, Xiao-Hu
Xu, Hang
Ding, Yi
Li, Yu-Wen
Wen, Ai-Dong
Differential gene expression profiles between two subtypes of ischemic stroke with blood stasis syndromes
title Differential gene expression profiles between two subtypes of ischemic stroke with blood stasis syndromes
title_full Differential gene expression profiles between two subtypes of ischemic stroke with blood stasis syndromes
title_fullStr Differential gene expression profiles between two subtypes of ischemic stroke with blood stasis syndromes
title_full_unstemmed Differential gene expression profiles between two subtypes of ischemic stroke with blood stasis syndromes
title_short Differential gene expression profiles between two subtypes of ischemic stroke with blood stasis syndromes
title_sort differential gene expression profiles between two subtypes of ischemic stroke with blood stasis syndromes
topic Research Paper
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5762346/
https://www.ncbi.nlm.nih.gov/pubmed/29340078
http://dx.doi.org/10.18632/oncotarget.22877
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