The Transcriptome Characteristics of Severe Asthma From the Prospect of Co-Expressed Gene Modules

Rationale: Severe asthma is a heterogeneous disease with multiple molecular mechanisms. Gene expression studies of asthmatic bronchial epithelial cells have provided biological insights and underscored possible pathological mechanisms; however, the molecular basis in severe asthma is still poorly understood.Objective: The objective of this study was to identify the features of asthma and uncover the molecular basis of severe asthma in distinct molecular phenotype.Methods: The k-means clustering and differentially expressed genes (DEGs) were performed in 129 asthma individuals in the Severe Asthma Research Program. The DEG profiles were analyzed by weighted gene co-expression network analysis (WGCNA), and the expression value of each gene module in each individual was annotated by gene set variation analysis (GSVA).Results: Expression analysis defined five stable asthma subtype (AS): 1) Phagocytosis-Th2, 2) Normal-like, 3) Neutrophils, 4) Mucin-Th2, and 5) Interferon-Th1 and 15 co-expressed gene modules. “Phagocytosis-Th2” enriched for receptor-mediated endocytosis, upregulation of Toll-like receptor signal, and myeloid leukocyte activation. “Normal-like” is most similar to normal samples. “Mucin-Th2” preferentially expressed genes involved in O-glycan biosynthesis and unfolded protein response. “Interferon-Th1” displayed upregulation of genes that regulate networks involved in cell cycle, IFN gamma response, and CD8 TCR. The dysregulation of neural signal, REDOX, apoptosis, and O-glycan process were related to the severity of asthma. In non-TH2 subtype (Neutrophils and Interferon-Th1) with severe asthma individuals, the neural signals and IL26-related co-expression module were dysregulated more significantly compared to that in non-severe asthma. These data infer differences in the molecular evolution of asthma subtypes and identify opportunities for therapeutic development.Conclusions: Asthma is a heterogeneous disease. The co-expression analysis provides new insights into the biological mechanisms related to its phenotypes and the severity. Ausführliche Beschreibung

Gespeichert in:

Autor*in:	Bin Li [verfasserIn] Wen-Xuan Sun [verfasserIn] Wan-Ying Zhang [verfasserIn] Ye Zheng [verfasserIn] Lu Qiao [verfasserIn] Yue-Ming Hu [verfasserIn] Wei-Qiang Li [verfasserIn] Di Liu [verfasserIn] Bing Leng [verfasserIn] Jia-Ren Liu [verfasserIn] Xiao-Feng Jiang [verfasserIn] Yan Zhang [verfasserIn]

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2021

Schlagwörter:	Phagocytosis-Th2 normal-like neutrophils mucin-Th2 Interferon-Th1

Übergeordnetes Werk:	In: Frontiers in Genetics - Frontiers Media S.A., 2011, 12(2021)
Übergeordnetes Werk:	volume:12 ; year:2021

Links:	Link aufrufen Link aufrufen Link aufrufen Journal toc

DOI / URN:	10.3389/fgene.2021.765400

Katalog-ID:	DOAJ071836012

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allfields	10.3389/fgene.2021.765400 doi (DE-627)DOAJ071836012 (DE-599)DOAJa019f008fed341519ba3e07f65c7767f DE-627 ger DE-627 rakwb eng QH426-470 Bin Li verfasserin aut The Transcriptome Characteristics of Severe Asthma From the Prospect of Co-Expressed Gene Modules 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Rationale: Severe asthma is a heterogeneous disease with multiple molecular mechanisms. Gene expression studies of asthmatic bronchial epithelial cells have provided biological insights and underscored possible pathological mechanisms; however, the molecular basis in severe asthma is still poorly understood.Objective: The objective of this study was to identify the features of asthma and uncover the molecular basis of severe asthma in distinct molecular phenotype.Methods: The k-means clustering and differentially expressed genes (DEGs) were performed in 129 asthma individuals in the Severe Asthma Research Program. The DEG profiles were analyzed by weighted gene co-expression network analysis (WGCNA), and the expression value of each gene module in each individual was annotated by gene set variation analysis (GSVA).Results: Expression analysis defined five stable asthma subtype (AS): 1) Phagocytosis-Th2, 2) Normal-like, 3) Neutrophils, 4) Mucin-Th2, and 5) Interferon-Th1 and 15 co-expressed gene modules. “Phagocytosis-Th2” enriched for receptor-mediated endocytosis, upregulation of Toll-like receptor signal, and myeloid leukocyte activation. “Normal-like” is most similar to normal samples. “Mucin-Th2” preferentially expressed genes involved in O-glycan biosynthesis and unfolded protein response. “Interferon-Th1” displayed upregulation of genes that regulate networks involved in cell cycle, IFN gamma response, and CD8 TCR. The dysregulation of neural signal, REDOX, apoptosis, and O-glycan process were related to the severity of asthma. In non-TH2 subtype (Neutrophils and Interferon-Th1) with severe asthma individuals, the neural signals and IL26-related co-expression module were dysregulated more significantly compared to that in non-severe asthma. These data infer differences in the molecular evolution of asthma subtypes and identify opportunities for therapeutic development.Conclusions: Asthma is a heterogeneous disease. The co-expression analysis provides new insights into the biological mechanisms related to its phenotypes and the severity. Phagocytosis-Th2 normal-like neutrophils mucin-Th2 Interferon-Th1 Genetics Bin Li verfasserin aut Bin Li verfasserin aut Wen-Xuan Sun verfasserin aut Wan-Ying Zhang verfasserin aut Wan-Ying Zhang verfasserin aut Ye Zheng verfasserin aut Lu Qiao verfasserin aut Yue-Ming Hu verfasserin aut Wei-Qiang Li verfasserin aut Di Liu verfasserin aut Bing Leng verfasserin aut Jia-Ren Liu verfasserin aut Jia-Ren Liu verfasserin aut Xiao-Feng Jiang verfasserin aut Yan Zhang verfasserin aut In Frontiers in Genetics Frontiers Media S.A., 2011 12(2021) (DE-627)65799829X (DE-600)2606823-0 16648021 nnns volume:12 year:2021 https://doi.org/10.3389/fgene.2021.765400 kostenfrei https://doaj.org/article/a019f008fed341519ba3e07f65c7767f kostenfrei https://www.frontiersin.org/articles/10.3389/fgene.2021.765400/full kostenfrei https://doaj.org/toc/1664-8021 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 12 2021
spelling	10.3389/fgene.2021.765400 doi (DE-627)DOAJ071836012 (DE-599)DOAJa019f008fed341519ba3e07f65c7767f DE-627 ger DE-627 rakwb eng QH426-470 Bin Li verfasserin aut The Transcriptome Characteristics of Severe Asthma From the Prospect of Co-Expressed Gene Modules 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Rationale: Severe asthma is a heterogeneous disease with multiple molecular mechanisms. Gene expression studies of asthmatic bronchial epithelial cells have provided biological insights and underscored possible pathological mechanisms; however, the molecular basis in severe asthma is still poorly understood.Objective: The objective of this study was to identify the features of asthma and uncover the molecular basis of severe asthma in distinct molecular phenotype.Methods: The k-means clustering and differentially expressed genes (DEGs) were performed in 129 asthma individuals in the Severe Asthma Research Program. The DEG profiles were analyzed by weighted gene co-expression network analysis (WGCNA), and the expression value of each gene module in each individual was annotated by gene set variation analysis (GSVA).Results: Expression analysis defined five stable asthma subtype (AS): 1) Phagocytosis-Th2, 2) Normal-like, 3) Neutrophils, 4) Mucin-Th2, and 5) Interferon-Th1 and 15 co-expressed gene modules. “Phagocytosis-Th2” enriched for receptor-mediated endocytosis, upregulation of Toll-like receptor signal, and myeloid leukocyte activation. “Normal-like” is most similar to normal samples. “Mucin-Th2” preferentially expressed genes involved in O-glycan biosynthesis and unfolded protein response. “Interferon-Th1” displayed upregulation of genes that regulate networks involved in cell cycle, IFN gamma response, and CD8 TCR. The dysregulation of neural signal, REDOX, apoptosis, and O-glycan process were related to the severity of asthma. In non-TH2 subtype (Neutrophils and Interferon-Th1) with severe asthma individuals, the neural signals and IL26-related co-expression module were dysregulated more significantly compared to that in non-severe asthma. These data infer differences in the molecular evolution of asthma subtypes and identify opportunities for therapeutic development.Conclusions: Asthma is a heterogeneous disease. The co-expression analysis provides new insights into the biological mechanisms related to its phenotypes and the severity. Phagocytosis-Th2 normal-like neutrophils mucin-Th2 Interferon-Th1 Genetics Bin Li verfasserin aut Bin Li verfasserin aut Wen-Xuan Sun verfasserin aut Wan-Ying Zhang verfasserin aut Wan-Ying Zhang verfasserin aut Ye Zheng verfasserin aut Lu Qiao verfasserin aut Yue-Ming Hu verfasserin aut Wei-Qiang Li verfasserin aut Di Liu verfasserin aut Bing Leng verfasserin aut Jia-Ren Liu verfasserin aut Jia-Ren Liu verfasserin aut Xiao-Feng Jiang verfasserin aut Yan Zhang verfasserin aut In Frontiers in Genetics Frontiers Media S.A., 2011 12(2021) (DE-627)65799829X (DE-600)2606823-0 16648021 nnns volume:12 year:2021 https://doi.org/10.3389/fgene.2021.765400 kostenfrei https://doaj.org/article/a019f008fed341519ba3e07f65c7767f kostenfrei https://www.frontiersin.org/articles/10.3389/fgene.2021.765400/full kostenfrei https://doaj.org/toc/1664-8021 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 12 2021
allfields_unstemmed	10.3389/fgene.2021.765400 doi (DE-627)DOAJ071836012 (DE-599)DOAJa019f008fed341519ba3e07f65c7767f DE-627 ger DE-627 rakwb eng QH426-470 Bin Li verfasserin aut The Transcriptome Characteristics of Severe Asthma From the Prospect of Co-Expressed Gene Modules 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Rationale: Severe asthma is a heterogeneous disease with multiple molecular mechanisms. Gene expression studies of asthmatic bronchial epithelial cells have provided biological insights and underscored possible pathological mechanisms; however, the molecular basis in severe asthma is still poorly understood.Objective: The objective of this study was to identify the features of asthma and uncover the molecular basis of severe asthma in distinct molecular phenotype.Methods: The k-means clustering and differentially expressed genes (DEGs) were performed in 129 asthma individuals in the Severe Asthma Research Program. The DEG profiles were analyzed by weighted gene co-expression network analysis (WGCNA), and the expression value of each gene module in each individual was annotated by gene set variation analysis (GSVA).Results: Expression analysis defined five stable asthma subtype (AS): 1) Phagocytosis-Th2, 2) Normal-like, 3) Neutrophils, 4) Mucin-Th2, and 5) Interferon-Th1 and 15 co-expressed gene modules. “Phagocytosis-Th2” enriched for receptor-mediated endocytosis, upregulation of Toll-like receptor signal, and myeloid leukocyte activation. “Normal-like” is most similar to normal samples. “Mucin-Th2” preferentially expressed genes involved in O-glycan biosynthesis and unfolded protein response. “Interferon-Th1” displayed upregulation of genes that regulate networks involved in cell cycle, IFN gamma response, and CD8 TCR. The dysregulation of neural signal, REDOX, apoptosis, and O-glycan process were related to the severity of asthma. In non-TH2 subtype (Neutrophils and Interferon-Th1) with severe asthma individuals, the neural signals and IL26-related co-expression module were dysregulated more significantly compared to that in non-severe asthma. These data infer differences in the molecular evolution of asthma subtypes and identify opportunities for therapeutic development.Conclusions: Asthma is a heterogeneous disease. The co-expression analysis provides new insights into the biological mechanisms related to its phenotypes and the severity. Phagocytosis-Th2 normal-like neutrophils mucin-Th2 Interferon-Th1 Genetics Bin Li verfasserin aut Bin Li verfasserin aut Wen-Xuan Sun verfasserin aut Wan-Ying Zhang verfasserin aut Wan-Ying Zhang verfasserin aut Ye Zheng verfasserin aut Lu Qiao verfasserin aut Yue-Ming Hu verfasserin aut Wei-Qiang Li verfasserin aut Di Liu verfasserin aut Bing Leng verfasserin aut Jia-Ren Liu verfasserin aut Jia-Ren Liu verfasserin aut Xiao-Feng Jiang verfasserin aut Yan Zhang verfasserin aut In Frontiers in Genetics Frontiers Media S.A., 2011 12(2021) (DE-627)65799829X (DE-600)2606823-0 16648021 nnns volume:12 year:2021 https://doi.org/10.3389/fgene.2021.765400 kostenfrei https://doaj.org/article/a019f008fed341519ba3e07f65c7767f kostenfrei https://www.frontiersin.org/articles/10.3389/fgene.2021.765400/full kostenfrei https://doaj.org/toc/1664-8021 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 12 2021
allfieldsGer	10.3389/fgene.2021.765400 doi (DE-627)DOAJ071836012 (DE-599)DOAJa019f008fed341519ba3e07f65c7767f DE-627 ger DE-627 rakwb eng QH426-470 Bin Li verfasserin aut The Transcriptome Characteristics of Severe Asthma From the Prospect of Co-Expressed Gene Modules 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Rationale: Severe asthma is a heterogeneous disease with multiple molecular mechanisms. Gene expression studies of asthmatic bronchial epithelial cells have provided biological insights and underscored possible pathological mechanisms; however, the molecular basis in severe asthma is still poorly understood.Objective: The objective of this study was to identify the features of asthma and uncover the molecular basis of severe asthma in distinct molecular phenotype.Methods: The k-means clustering and differentially expressed genes (DEGs) were performed in 129 asthma individuals in the Severe Asthma Research Program. The DEG profiles were analyzed by weighted gene co-expression network analysis (WGCNA), and the expression value of each gene module in each individual was annotated by gene set variation analysis (GSVA).Results: Expression analysis defined five stable asthma subtype (AS): 1) Phagocytosis-Th2, 2) Normal-like, 3) Neutrophils, 4) Mucin-Th2, and 5) Interferon-Th1 and 15 co-expressed gene modules. “Phagocytosis-Th2” enriched for receptor-mediated endocytosis, upregulation of Toll-like receptor signal, and myeloid leukocyte activation. “Normal-like” is most similar to normal samples. “Mucin-Th2” preferentially expressed genes involved in O-glycan biosynthesis and unfolded protein response. “Interferon-Th1” displayed upregulation of genes that regulate networks involved in cell cycle, IFN gamma response, and CD8 TCR. The dysregulation of neural signal, REDOX, apoptosis, and O-glycan process were related to the severity of asthma. In non-TH2 subtype (Neutrophils and Interferon-Th1) with severe asthma individuals, the neural signals and IL26-related co-expression module were dysregulated more significantly compared to that in non-severe asthma. These data infer differences in the molecular evolution of asthma subtypes and identify opportunities for therapeutic development.Conclusions: Asthma is a heterogeneous disease. The co-expression analysis provides new insights into the biological mechanisms related to its phenotypes and the severity. Phagocytosis-Th2 normal-like neutrophils mucin-Th2 Interferon-Th1 Genetics Bin Li verfasserin aut Bin Li verfasserin aut Wen-Xuan Sun verfasserin aut Wan-Ying Zhang verfasserin aut Wan-Ying Zhang verfasserin aut Ye Zheng verfasserin aut Lu Qiao verfasserin aut Yue-Ming Hu verfasserin aut Wei-Qiang Li verfasserin aut Di Liu verfasserin aut Bing Leng verfasserin aut Jia-Ren Liu verfasserin aut Jia-Ren Liu verfasserin aut Xiao-Feng Jiang verfasserin aut Yan Zhang verfasserin aut In Frontiers in Genetics Frontiers Media S.A., 2011 12(2021) (DE-627)65799829X (DE-600)2606823-0 16648021 nnns volume:12 year:2021 https://doi.org/10.3389/fgene.2021.765400 kostenfrei https://doaj.org/article/a019f008fed341519ba3e07f65c7767f kostenfrei https://www.frontiersin.org/articles/10.3389/fgene.2021.765400/full kostenfrei https://doaj.org/toc/1664-8021 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 12 2021
allfieldsSound	10.3389/fgene.2021.765400 doi (DE-627)DOAJ071836012 (DE-599)DOAJa019f008fed341519ba3e07f65c7767f DE-627 ger DE-627 rakwb eng QH426-470 Bin Li verfasserin aut The Transcriptome Characteristics of Severe Asthma From the Prospect of Co-Expressed Gene Modules 2021 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier Rationale: Severe asthma is a heterogeneous disease with multiple molecular mechanisms. Gene expression studies of asthmatic bronchial epithelial cells have provided biological insights and underscored possible pathological mechanisms; however, the molecular basis in severe asthma is still poorly understood.Objective: The objective of this study was to identify the features of asthma and uncover the molecular basis of severe asthma in distinct molecular phenotype.Methods: The k-means clustering and differentially expressed genes (DEGs) were performed in 129 asthma individuals in the Severe Asthma Research Program. The DEG profiles were analyzed by weighted gene co-expression network analysis (WGCNA), and the expression value of each gene module in each individual was annotated by gene set variation analysis (GSVA).Results: Expression analysis defined five stable asthma subtype (AS): 1) Phagocytosis-Th2, 2) Normal-like, 3) Neutrophils, 4) Mucin-Th2, and 5) Interferon-Th1 and 15 co-expressed gene modules. “Phagocytosis-Th2” enriched for receptor-mediated endocytosis, upregulation of Toll-like receptor signal, and myeloid leukocyte activation. “Normal-like” is most similar to normal samples. “Mucin-Th2” preferentially expressed genes involved in O-glycan biosynthesis and unfolded protein response. “Interferon-Th1” displayed upregulation of genes that regulate networks involved in cell cycle, IFN gamma response, and CD8 TCR. The dysregulation of neural signal, REDOX, apoptosis, and O-glycan process were related to the severity of asthma. In non-TH2 subtype (Neutrophils and Interferon-Th1) with severe asthma individuals, the neural signals and IL26-related co-expression module were dysregulated more significantly compared to that in non-severe asthma. These data infer differences in the molecular evolution of asthma subtypes and identify opportunities for therapeutic development.Conclusions: Asthma is a heterogeneous disease. The co-expression analysis provides new insights into the biological mechanisms related to its phenotypes and the severity. Phagocytosis-Th2 normal-like neutrophils mucin-Th2 Interferon-Th1 Genetics Bin Li verfasserin aut Bin Li verfasserin aut Wen-Xuan Sun verfasserin aut Wan-Ying Zhang verfasserin aut Wan-Ying Zhang verfasserin aut Ye Zheng verfasserin aut Lu Qiao verfasserin aut Yue-Ming Hu verfasserin aut Wei-Qiang Li verfasserin aut Di Liu verfasserin aut Bing Leng verfasserin aut Jia-Ren Liu verfasserin aut Jia-Ren Liu verfasserin aut Xiao-Feng Jiang verfasserin aut Yan Zhang verfasserin aut In Frontiers in Genetics Frontiers Media S.A., 2011 12(2021) (DE-627)65799829X (DE-600)2606823-0 16648021 nnns volume:12 year:2021 https://doi.org/10.3389/fgene.2021.765400 kostenfrei https://doaj.org/article/a019f008fed341519ba3e07f65c7767f kostenfrei https://www.frontiersin.org/articles/10.3389/fgene.2021.765400/full kostenfrei https://doaj.org/toc/1664-8021 Journal toc kostenfrei GBV_USEFLAG_A SYSFLAG_A GBV_DOAJ SSG-OLC-PHA GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_39 GBV_ILN_40 GBV_ILN_62 GBV_ILN_63 GBV_ILN_65 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_95 GBV_ILN_105 GBV_ILN_110 GBV_ILN_151 GBV_ILN_161 GBV_ILN_170 GBV_ILN_213 GBV_ILN_230 GBV_ILN_285 GBV_ILN_293 GBV_ILN_602 GBV_ILN_2003 GBV_ILN_2014 GBV_ILN_4012 GBV_ILN_4037 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4249 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4338 GBV_ILN_4367 GBV_ILN_4700 AR 12 2021
language	English
source	In Frontiers in Genetics 12(2021) volume:12 year:2021
sourceStr	In Frontiers in Genetics 12(2021) volume:12 year:2021
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	Phagocytosis-Th2 normal-like neutrophils mucin-Th2 Interferon-Th1 Genetics
isfreeaccess_bool	true
container_title	Frontiers in Genetics
authorswithroles_txt_mv	Bin Li @@aut@@ Wen-Xuan Sun @@aut@@ Wan-Ying Zhang @@aut@@ Ye Zheng @@aut@@ Lu Qiao @@aut@@ Yue-Ming Hu @@aut@@ Wei-Qiang Li @@aut@@ Di Liu @@aut@@ Bing Leng @@aut@@ Jia-Ren Liu @@aut@@ Xiao-Feng Jiang @@aut@@ Yan Zhang @@aut@@
publishDateDaySort_date	2021-01-01T00:00:00Z
hierarchy_top_id	65799829X
id	DOAJ071836012
language_de	englisch
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The DEG profiles were analyzed by weighted gene co-expression network analysis (WGCNA), and the expression value of each gene module in each individual was annotated by gene set variation analysis (GSVA).Results: Expression analysis defined five stable asthma subtype (AS): 1) Phagocytosis-Th2, 2) Normal-like, 3) Neutrophils, 4) Mucin-Th2, and 5) Interferon-Th1 and 15 co-expressed gene modules. “Phagocytosis-Th2” enriched for receptor-mediated endocytosis, upregulation of Toll-like receptor signal, and myeloid leukocyte activation. “Normal-like” is most similar to normal samples. “Mucin-Th2” preferentially expressed genes involved in O-glycan biosynthesis and unfolded protein response. “Interferon-Th1” displayed upregulation of genes that regulate networks involved in cell cycle, IFN gamma response, and CD8 TCR. The dysregulation of neural signal, REDOX, apoptosis, and O-glycan process were related to the severity of asthma. In non-TH2 subtype (Neutrophils and Interferon-Th1) with severe asthma individuals, the neural signals and IL26-related co-expression module were dysregulated more significantly compared to that in non-severe asthma. These data infer differences in the molecular evolution of asthma subtypes and identify opportunities for therapeutic development.Conclusions: Asthma is a heterogeneous disease. 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callnumber-first	Q - Science
author	Bin Li
spellingShingle	Bin Li misc QH426-470 misc Phagocytosis-Th2 misc normal-like misc neutrophils misc mucin-Th2 misc Interferon-Th1 misc Genetics The Transcriptome Characteristics of Severe Asthma From the Prospect of Co-Expressed Gene Modules
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topic_title	QH426-470 The Transcriptome Characteristics of Severe Asthma From the Prospect of Co-Expressed Gene Modules Phagocytosis-Th2 normal-like neutrophils mucin-Th2 Interferon-Th1
topic	misc QH426-470 misc Phagocytosis-Th2 misc normal-like misc neutrophils misc mucin-Th2 misc Interferon-Th1 misc Genetics
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title	The Transcriptome Characteristics of Severe Asthma From the Prospect of Co-Expressed Gene Modules
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title_full	The Transcriptome Characteristics of Severe Asthma From the Prospect of Co-Expressed Gene Modules
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author_browse	Bin Li Wen-Xuan Sun Wan-Ying Zhang Ye Zheng Lu Qiao Yue-Ming Hu Wei-Qiang Li Di Liu Bing Leng Jia-Ren Liu Xiao-Feng Jiang Yan Zhang
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title_sort	transcriptome characteristics of severe asthma from the prospect of co-expressed gene modules
callnumber	QH426-470
title_auth	The Transcriptome Characteristics of Severe Asthma From the Prospect of Co-Expressed Gene Modules
abstract	Rationale: Severe asthma is a heterogeneous disease with multiple molecular mechanisms. Gene expression studies of asthmatic bronchial epithelial cells have provided biological insights and underscored possible pathological mechanisms; however, the molecular basis in severe asthma is still poorly understood.Objective: The objective of this study was to identify the features of asthma and uncover the molecular basis of severe asthma in distinct molecular phenotype.Methods: The k-means clustering and differentially expressed genes (DEGs) were performed in 129 asthma individuals in the Severe Asthma Research Program. The DEG profiles were analyzed by weighted gene co-expression network analysis (WGCNA), and the expression value of each gene module in each individual was annotated by gene set variation analysis (GSVA).Results: Expression analysis defined five stable asthma subtype (AS): 1) Phagocytosis-Th2, 2) Normal-like, 3) Neutrophils, 4) Mucin-Th2, and 5) Interferon-Th1 and 15 co-expressed gene modules. “Phagocytosis-Th2” enriched for receptor-mediated endocytosis, upregulation of Toll-like receptor signal, and myeloid leukocyte activation. “Normal-like” is most similar to normal samples. “Mucin-Th2” preferentially expressed genes involved in O-glycan biosynthesis and unfolded protein response. “Interferon-Th1” displayed upregulation of genes that regulate networks involved in cell cycle, IFN gamma response, and CD8 TCR. The dysregulation of neural signal, REDOX, apoptosis, and O-glycan process were related to the severity of asthma. In non-TH2 subtype (Neutrophils and Interferon-Th1) with severe asthma individuals, the neural signals and IL26-related co-expression module were dysregulated more significantly compared to that in non-severe asthma. These data infer differences in the molecular evolution of asthma subtypes and identify opportunities for therapeutic development.Conclusions: Asthma is a heterogeneous disease. The co-expression analysis provides new insights into the biological mechanisms related to its phenotypes and the severity.
abstractGer	Rationale: Severe asthma is a heterogeneous disease with multiple molecular mechanisms. Gene expression studies of asthmatic bronchial epithelial cells have provided biological insights and underscored possible pathological mechanisms; however, the molecular basis in severe asthma is still poorly understood.Objective: The objective of this study was to identify the features of asthma and uncover the molecular basis of severe asthma in distinct molecular phenotype.Methods: The k-means clustering and differentially expressed genes (DEGs) were performed in 129 asthma individuals in the Severe Asthma Research Program. The DEG profiles were analyzed by weighted gene co-expression network analysis (WGCNA), and the expression value of each gene module in each individual was annotated by gene set variation analysis (GSVA).Results: Expression analysis defined five stable asthma subtype (AS): 1) Phagocytosis-Th2, 2) Normal-like, 3) Neutrophils, 4) Mucin-Th2, and 5) Interferon-Th1 and 15 co-expressed gene modules. “Phagocytosis-Th2” enriched for receptor-mediated endocytosis, upregulation of Toll-like receptor signal, and myeloid leukocyte activation. “Normal-like” is most similar to normal samples. “Mucin-Th2” preferentially expressed genes involved in O-glycan biosynthesis and unfolded protein response. “Interferon-Th1” displayed upregulation of genes that regulate networks involved in cell cycle, IFN gamma response, and CD8 TCR. The dysregulation of neural signal, REDOX, apoptosis, and O-glycan process were related to the severity of asthma. In non-TH2 subtype (Neutrophils and Interferon-Th1) with severe asthma individuals, the neural signals and IL26-related co-expression module were dysregulated more significantly compared to that in non-severe asthma. These data infer differences in the molecular evolution of asthma subtypes and identify opportunities for therapeutic development.Conclusions: Asthma is a heterogeneous disease. The co-expression analysis provides new insights into the biological mechanisms related to its phenotypes and the severity.
abstract_unstemmed	Rationale: Severe asthma is a heterogeneous disease with multiple molecular mechanisms. Gene expression studies of asthmatic bronchial epithelial cells have provided biological insights and underscored possible pathological mechanisms; however, the molecular basis in severe asthma is still poorly understood.Objective: The objective of this study was to identify the features of asthma and uncover the molecular basis of severe asthma in distinct molecular phenotype.Methods: The k-means clustering and differentially expressed genes (DEGs) were performed in 129 asthma individuals in the Severe Asthma Research Program. The DEG profiles were analyzed by weighted gene co-expression network analysis (WGCNA), and the expression value of each gene module in each individual was annotated by gene set variation analysis (GSVA).Results: Expression analysis defined five stable asthma subtype (AS): 1) Phagocytosis-Th2, 2) Normal-like, 3) Neutrophils, 4) Mucin-Th2, and 5) Interferon-Th1 and 15 co-expressed gene modules. “Phagocytosis-Th2” enriched for receptor-mediated endocytosis, upregulation of Toll-like receptor signal, and myeloid leukocyte activation. “Normal-like” is most similar to normal samples. “Mucin-Th2” preferentially expressed genes involved in O-glycan biosynthesis and unfolded protein response. “Interferon-Th1” displayed upregulation of genes that regulate networks involved in cell cycle, IFN gamma response, and CD8 TCR. The dysregulation of neural signal, REDOX, apoptosis, and O-glycan process were related to the severity of asthma. In non-TH2 subtype (Neutrophils and Interferon-Th1) with severe asthma individuals, the neural signals and IL26-related co-expression module were dysregulated more significantly compared to that in non-severe asthma. These data infer differences in the molecular evolution of asthma subtypes and identify opportunities for therapeutic development.Conclusions: Asthma is a heterogeneous disease. The co-expression analysis provides new insights into the biological mechanisms related to its phenotypes and the severity.
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title_short	The Transcriptome Characteristics of Severe Asthma From the Prospect of Co-Expressed Gene Modules
url	https://doi.org/10.3389/fgene.2021.765400 https://doaj.org/article/a019f008fed341519ba3e07f65c7767f https://www.frontiersin.org/articles/10.3389/fgene.2021.765400/full https://doaj.org/toc/1664-8021
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author2	Bin Li Wen-Xuan Sun Wan-Ying Zhang Ye Zheng Lu Qiao Yue-Ming Hu Wei-Qiang Li Di Liu Bing Leng Jia-Ren Liu Xiao-Feng Jiang Yan Zhang
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doi_str	10.3389/fgene.2021.765400
callnumber-a	QH426-470
up_date	2024-07-03T22:26:26.014Z
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