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Gene expression profiling of idiopathic interstitial pneumonias (IIPs): identification of potential diagnostic markers and therapeutic targets

https://hiroshima.repo.nii.ac.jp/records/2006515
https://hiroshima.repo.nii.ac.jp/records/2006515
bfdd45f4-1e86-4a07-99d6-cad6136cb98a
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bmcmg_18_88.pdf bmcmg_18_88.pdf (1008.4 KB)
Item type デフォルトアイテムタイプ_(フル)(1)
公開日 2023-03-18
タイトル
タイトル Gene expression profiling of idiopathic interstitial pneumonias (IIPs): identification of potential diagnostic markers and therapeutic targets
言語 en
作成者 Horimasu, Yasushi

× Horimasu, Yasushi

en Horimasu, Yasushi

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Ishikawa, Nobuhisa

× Ishikawa, Nobuhisa

en Ishikawa, Nobuhisa

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Taniwaki, Masaya

× Taniwaki, Masaya

en Taniwaki, Masaya

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Yamaguchi, Kakuhiro

× Yamaguchi, Kakuhiro

en Yamaguchi, Kakuhiro

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Hamai, Kosuke

× Hamai, Kosuke

en Hamai, Kosuke

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Iwamoto, Hiroshi

× Iwamoto, Hiroshi

en Iwamoto, Hiroshi

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Ohshimo, Shinichiro

× Ohshimo, Shinichiro

en Ohshimo, Shinichiro

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Hamada, Hironobu

× Hamada, Hironobu

en Hamada, Hironobu

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Hattori, Noboru

× Hattori, Noboru

en Hattori, Noboru

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Okada, Morihito

× Okada, Morihito

en Okada, Morihito

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Arihiro, Koji

× Arihiro, Koji

en Arihiro, Koji

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Ohtsuki, Yuji

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en Ohtsuki, Yuji

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Kohno, Nobuoki

× Kohno, Nobuoki

en Kohno, Nobuoki

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アクセス権
アクセス権 open access
アクセス権URI http://purl.org/coar/access_right/c_abf2
権利情報
権利情報 © The Author(s). 2017. This article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated.
内容記述
内容記述 Background: Chronic fibrosing idiopathic interstitial pneumonia (IIP) is characterized by alveolar epithelial damage, activation of fibroblast proliferation, and loss of normal pulmonary architecture and function. This study aims to investigate the genetic backgrounds of IIP through gene expression profiling and pathway analysis, and to identify potential biomarkers that can aid in diagnosis and serve as novel therapeutic targets. Methods:RNA extracted from lung specimens of 12 patients with chronic fibrosing IIP was profiled using Illumina Human WG-6 v3 BeadChips, and Ingenuity Pathway Analysis was performed to identify altered functional and canonical signaling pathways. For validating the results from gene expression analysis, immunohistochemical staining of 10 patients with chronic fibrosing IIP was performed. Results: Ninety-eight genes were upregulated in IIP patients relative to control subjects. Some of the upregulated genes, namely desmoglein 3 (DSG3), protocadherin gamma-A9 (PCDHGA9) and discoidin domain-containing receptor 1 (DDR1) are implicated in cell-cell interaction and/or adhesion; some, namely collagen type VII, alpha 1 (COL7A1), contactin-associated protein-like 3B (CNTNAP3B) and mucin-1 (MUC1) are encoding the extracellular matrix molecule or the molecules involved in cell-matrix interactions; and the others, namely CDC25C and growth factor independent protein 1B (GFI1B) are known to affect cell proliferation by affecting the progression of cell cycle or regulating transcription. According to pathway analysis, alternated pathways in IIP were related to cell death and survival and cellular growth and proliferation, which are more similar to cancer than to inflammatory response and immunological diseases. Using immunohistochemistry, we further validate that DSG3, the most highly upregulated gene, shows higher expression in chronic fibrosing IIP lung as compared to control lung. Conclusion: We identified several genes upregulated in chronic fibrosing IIP patients as compared to control, and found genes and pathways implicated in cancer, rather than in inflammatory or immunological disease to play important roles in the pathogenesis of IIPs. Moreover, DSG3 is a novel potential biomarker for chronic fibrosing IIP with its significantly high expression in IIP lung.
言語 en
内容記述
内容記述タイプ Other
内容記述 This work was supported by Grants-in-Aid for Scientific Research from the Ministry of Education, Culture, Sports, Science and Technology of Japan.
出版者
出版者 BioMed Central Ltd
言語
言語 eng
資源タイプ
資源タイプ識別子 http://purl.org/coar/resource_type/c_6501
資源タイプ journal article
出版タイプ
出版タイプ VoR
出版タイプResource http://purl.org/coar/version/c_970fb48d4fbd8a85
関連情報
識別子タイプ DOI
関連識別子 10.1186/s12881-017-0449-9
関連情報
識別子タイプ PMID
関連識別子 28821283
関連情報
識別子タイプ DOI
関連識別子 https://doi.org/10.1186/s12881-017-0449-9
収録物識別子
収録物識別子タイプ ISSN
収録物識別子 1471-2350
開始ページ
開始ページ 88
書誌情報 BMC Medical Genetics
BMC Medical Genetics

巻 18, p. 88, 発行日 2017-08-18
旧ID 48671
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