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Circulating MicroRNA Profiles Differ between Qi-Stagnation and Qi-Deficiency in Coronary Heart Disease Patients with Blood Stasis Syndrome

We compared the circulating microRNA profiles of Qi-stagnation (QSB) and Qi-deficiency (QDB) in coronary heart disease (CHD) patients with blood stasis syndrome. Twenty-nine CHD patients were divided into QSB group and QDB group. The analysis was carried out through comparing their circulating micro...

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Detalles Bibliográficos
Autores principales: Hou, Jincai, Wang, Jun, Lin, Chengren, Fu, Jianhua, Ren, Jianxun, Li, Lei, Guo, Hao, Han, Xiao, Liu, Jianxun
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Hindawi Publishing Corporation 2014
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4273468/
https://www.ncbi.nlm.nih.gov/pubmed/25548593
http://dx.doi.org/10.1155/2014/926962
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author Hou, Jincai
Wang, Jun
Lin, Chengren
Fu, Jianhua
Ren, Jianxun
Li, Lei
Guo, Hao
Han, Xiao
Liu, Jianxun
author_facet Hou, Jincai
Wang, Jun
Lin, Chengren
Fu, Jianhua
Ren, Jianxun
Li, Lei
Guo, Hao
Han, Xiao
Liu, Jianxun
author_sort Hou, Jincai
collection PubMed
description We compared the circulating microRNA profiles of Qi-stagnation (QSB) and Qi-deficiency (QDB) in coronary heart disease (CHD) patients with blood stasis syndrome. Twenty-nine CHD patients were divided into QSB group and QDB group. The analysis was carried out through comparing their circulating microRNA profiles and the following bioinformatics analysis. The number of differential miRNAs in QDB group was much more than that in QSB group. Functional annotations of the differentially expressed miRNAs target genes in the QSB group and QDB group were, respectively, related to regulation of cellular component organization, regulation of glucose metabolic process, and so forth and protein kinase cascade, phosphate metabolic process, and so forth. KEGG pathway analysis showed that the process Qi-deficiency was associated with phagocytosis including endocytosis and mTOR signaling pathway. Specifically, pathway of cell adhesion molecules played the crucial role in the pathological process of Qi-stagnation, with a unique upregulation except for pathways associated with cancer signal. MicroRNA-gene-net analysis indicated that let-7c, miR-4487, miR-619, miR-8075, miR-6735, and miR-32-5p and miR-17-5p, miR-130a, and miR 320 family had the most important and extensive regulatory function for Qi-stagnation syndromes and Qi-deficiency syndromes, respectively. Differentially expressed miRNAs and concerned pathways suggest different molecular mechanisms that may mediate the pathological process of QSB and QDB syndromes.
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spelling pubmed-42734682014-12-29 Circulating MicroRNA Profiles Differ between Qi-Stagnation and Qi-Deficiency in Coronary Heart Disease Patients with Blood Stasis Syndrome Hou, Jincai Wang, Jun Lin, Chengren Fu, Jianhua Ren, Jianxun Li, Lei Guo, Hao Han, Xiao Liu, Jianxun Evid Based Complement Alternat Med Research Article We compared the circulating microRNA profiles of Qi-stagnation (QSB) and Qi-deficiency (QDB) in coronary heart disease (CHD) patients with blood stasis syndrome. Twenty-nine CHD patients were divided into QSB group and QDB group. The analysis was carried out through comparing their circulating microRNA profiles and the following bioinformatics analysis. The number of differential miRNAs in QDB group was much more than that in QSB group. Functional annotations of the differentially expressed miRNAs target genes in the QSB group and QDB group were, respectively, related to regulation of cellular component organization, regulation of glucose metabolic process, and so forth and protein kinase cascade, phosphate metabolic process, and so forth. KEGG pathway analysis showed that the process Qi-deficiency was associated with phagocytosis including endocytosis and mTOR signaling pathway. Specifically, pathway of cell adhesion molecules played the crucial role in the pathological process of Qi-stagnation, with a unique upregulation except for pathways associated with cancer signal. MicroRNA-gene-net analysis indicated that let-7c, miR-4487, miR-619, miR-8075, miR-6735, and miR-32-5p and miR-17-5p, miR-130a, and miR 320 family had the most important and extensive regulatory function for Qi-stagnation syndromes and Qi-deficiency syndromes, respectively. Differentially expressed miRNAs and concerned pathways suggest different molecular mechanisms that may mediate the pathological process of QSB and QDB syndromes. Hindawi Publishing Corporation 2014 2014-12-04 /pmc/articles/PMC4273468/ /pubmed/25548593 http://dx.doi.org/10.1155/2014/926962 Text en Copyright © 2014 Jincai Hou et al. https://creativecommons.org/licenses/by/3.0/ This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
spellingShingle Research Article
Hou, Jincai
Wang, Jun
Lin, Chengren
Fu, Jianhua
Ren, Jianxun
Li, Lei
Guo, Hao
Han, Xiao
Liu, Jianxun
Circulating MicroRNA Profiles Differ between Qi-Stagnation and Qi-Deficiency in Coronary Heart Disease Patients with Blood Stasis Syndrome
title Circulating MicroRNA Profiles Differ between Qi-Stagnation and Qi-Deficiency in Coronary Heart Disease Patients with Blood Stasis Syndrome
title_full Circulating MicroRNA Profiles Differ between Qi-Stagnation and Qi-Deficiency in Coronary Heart Disease Patients with Blood Stasis Syndrome
title_fullStr Circulating MicroRNA Profiles Differ between Qi-Stagnation and Qi-Deficiency in Coronary Heart Disease Patients with Blood Stasis Syndrome
title_full_unstemmed Circulating MicroRNA Profiles Differ between Qi-Stagnation and Qi-Deficiency in Coronary Heart Disease Patients with Blood Stasis Syndrome
title_short Circulating MicroRNA Profiles Differ between Qi-Stagnation and Qi-Deficiency in Coronary Heart Disease Patients with Blood Stasis Syndrome
title_sort circulating microrna profiles differ between qi-stagnation and qi-deficiency in coronary heart disease patients with blood stasis syndrome
topic Research Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4273468/
https://www.ncbi.nlm.nih.gov/pubmed/25548593
http://dx.doi.org/10.1155/2014/926962
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