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  1. 学術雑誌論文

Sphingomyelin maintains the cutaneous barrier via regulation of the STAT3 pathway

https://az.repo.nii.ac.jp/records/2000324
https://az.repo.nii.ac.jp/records/2000324
0d5e34a8-b333-4add-aa5f-90fb8e329ca2
名前 / ファイル ライセンス アクション
The The FASEB Journal - 2022 - Komuro - Sphingomyelin maintains the cutaneous barrier via regulation of the STAT3 pathway.pdf (1.6 MB)
Item type 学術雑誌論文 / Journal Article(1)
公開日 2025-02-28
タイトル
タイトル Sphingomyelin maintains the cutaneous barrier via regulation of the STAT3 pathway
言語 en
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
著者 Komuro, Mariko

× Komuro, Mariko

en Komuro, Mariko

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Nagane, Masaki

× Nagane, Masaki

en Nagane, Masaki

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Fukuyama, Tomoki

× Fukuyama, Tomoki

en Fukuyama, Tomoki

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Luo, Xiaolin

× Luo, Xiaolin

en Luo, Xiaolin

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Hiraki, Shinobu

× Hiraki, Shinobu

en Hiraki, Shinobu

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Miyanabe, Masakatsu

× Miyanabe, Masakatsu

en Miyanabe, Masakatsu

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Ishikawa, Miyuki

× Ishikawa, Miyuki

en Ishikawa, Miyuki

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Niwa, Chiaki

× Niwa, Chiaki

en Niwa, Chiaki

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Murakami, Hironobu

× Murakami, Hironobu

en Murakami, Hironobu

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Okamoto, Mariko

× Okamoto, Mariko

en Okamoto, Mariko

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Yamashita, Tadashi

× Yamashita, Tadashi

en Yamashita, Tadashi

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Abstract
内容記述タイプ Abstract
内容記述 Epidermal tissues play vital roles in maintaining homeostasis and preventing the dysregulation of the cutaneous barrier. Sphingomyelin (SM), a sphingolipid synthesized by sphingomyelin synthase (SMS) 1 and 2, is involved in signal transduction via modulation of lipid-raft functions. Though the implications of SMS on inflammatory diseases have been reported, its role in dermatitis has not been clarified. In this study, we investigated the role of SM in the cutaneous barrier using a dermatitis model established by employing Sgms1 and 2 deficient mice. SM deficiency impaired the cutaneous inflammation and upregulated signal transducer and activator of transcription 3 (STAT3) phosphorylation in epithelial tissues. Furthermore, using mouse embryonic fibroblast cells, the sensitivity of STAT3 to Interleukin-6 stimulation was increased in Sgms-deficient cells. Using tofacitinib, a clinical JAK inhibitor, the study showed that SM deficiency might participate in STAT3 phosphorylation via JAK activation. Overall, these results demonstrate that SM is essential for maintaining the cutaneous barrier via the STAT3 pathway, suggesting SM could be a potential therapeutic target for dermatitis treatment.
言語 en
書誌情報 FASEB journal : official publication of the Federation of American Societies for Experimental Biology

巻 36, 号 4, p. e22111, 発行日 2022-04
出版者
出版者 Wiley
DOI
識別子タイプ DOI
関連識別子 10.1096/fj.202100721RR
著者版フラグ
出版タイプ VoR
出版タイプResource http://purl.org/coar/version/c_970fb48d4fbd8a85
査読
内容記述タイプ Other
内容記述 査読あり
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