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  2. 国外雑誌論文

Ninjurin1 Deletion in NG2-Positive Pericytes Prevents Microvessel Maturation and Delays Wound Healing

https://asahikawa-med.repo.nii.ac.jp/records/2000531
https://asahikawa-med.repo.nii.ac.jp/records/2000531
51eb7917-0c18-42e8-9542-8bc910c29fd6
名前 / ファイル ライセンス アクション
36262667.pdf 36262667.pdf (10.1 MB)
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Item type 学術雑誌論文 / Journal Article_02(1)
公開日 2025-06-18
タイトル
タイトル Ninjurin1 Deletion in NG2-Positive Pericytes Prevents Microvessel Maturation and Delays Wound Healing
言語 en
言語
言語 eng
キーワード
主題Scheme Other
キーワード 3D, three-dimensional
キーワード
主題Scheme Other
キーワード EC, endothelial cell
キーワード
主題Scheme Other
キーワード KC, keratinocyte
キーワード
主題Scheme Other
キーワード KO, knockout
キーワード
主題Scheme Other
キーワード Ninj1, Ninjurin-1
キーワード
主題Scheme Other
キーワード PC, pericyte
キーワード
主題Scheme Other
キーワード Tam, tamoxifen
キーワード
主題Scheme Other
キーワード VSMC, vascular smooth muscle cell
キーワード
主題Scheme Other
キーワード WT, wild-type
資源タイプ
資源タイプ journal article
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
著者 Risa, Matsuo

× Risa, Matsuo

en Risa, Matsuo

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Mari, Kishibe

× Mari, Kishibe

en Mari, Kishibe

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Kiwamu, Horiuchi

× Kiwamu, Horiuchi

en Kiwamu, Horiuchi

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Kohei, Kano

× Kohei, Kano

en Kohei, Kano

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Takamitsu, Tatsukawa

× Takamitsu, Tatsukawa

en Takamitsu, Tatsukawa

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Taiki, Hayasaka

× Taiki, Hayasaka

en Taiki, Hayasaka

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Maki, Kabara

× Maki, Kabara

en Maki, Kabara

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Shin, Iinuma

× Shin, Iinuma

en Shin, Iinuma

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Ryoji, Eguchi

× Ryoji, Eguchi

en Ryoji, Eguchi

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Satomi, Igawa

× Satomi, Igawa

en Satomi, Igawa

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Naoyuki, Hasebe

× Naoyuki, Hasebe

en Naoyuki, Hasebe

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Akemi, Ishida-Yamamoto

× Akemi, Ishida-Yamamoto

en Akemi, Ishida-Yamamoto

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Jun-Ichi, Kawabe

× Jun-Ichi, Kawabe

en Jun-Ichi, Kawabe

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bibliographic_information en : JID innovations : skin science from molecules to population health.

巻 2, 号 6, p. 100141, 発行日 2022-07-07
ISSN
収録物識別子タイプ EISSN
収録物識別子 2667-0267
DOI
関連タイプ isIdenticalTo
識別子タイプ DOI
関連識別子 https://doi.org/10.1016/j.xjidi.2022.100141
リンクURL
内容記述タイプ Other
内容記述 https://www.sciencedirect.com/science/article/pii/S2667026722000492
言語 en
item_1716186501932
関連タイプ isIdenticalTo
識別子タイプ PMID
関連識別子 36262667
item_5_description_33
内容記述タイプ Abstract
内容記述 The formation of mature vasculature through angiogenesis is essential for adequate wound healing, such that blood-borne cells, nutrients, and oxygen can be delivered to the remodeling skin area. Neovessel maturation is highly dependent on the coordinated functions of vascular endothelial cells and perivascular cells, namely pericytes (PCs). However, the underlying mechanism for vascular maturation has not been completely elucidated, and its role in wound healing remains unclear. In this study, we investigated the role of Ninjurin-1 (Ninj1), a new molecule mediating vascular maturation, in wound healing using an inducible PC-specific Ninj1 deletion mouse model. Ninj1 expression increased temporarily in NG2-positive PCs in response to skin injury. When tamoxifen treatment induced a decreased Ninj1 expression in PCs, the neovessels in the regenerating wound margins were structurally and functionally immature, but the total number of microvessels was unaltered. This phenotypic change is associated with a reduction in PC-associated microvessels. Wound healing was significantly delayed in the NG2-specific Ninj1 deletion mouse model. Finally, we showed that Ninj1 is a crucial molecule that mediates vascular maturation in injured skin tissue through the interaction of vascular endothelial cells and PCs, thereby inducing adequate and prompt wound healing
言語 en
注記
内容記述タイプ Other
注記 © 2022. This manuscript version is made available under the CC-BY 4.0 license
https://creativecommons.org/licenses/by/4.0/
言語 en
出版タイプ
出版タイプ VoR
item_5_textarea_42
en
© 2022 The Authors.
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Cite as

Risa, Matsuo, Mari, Kishibe, Kiwamu, Horiuchi, Kohei, Kano, Takamitsu, Tatsukawa, Taiki, Hayasaka, Maki, Kabara, Shin, Iinuma, Ryoji, Eguchi, Satomi, Igawa, Naoyuki, Hasebe, Akemi, Ishida-Yamamoto, Jun-Ichi, Kawabe, n.d., Ninjurin1 Deletion in NG2-Positive Pericytes Prevents Microvessel Maturation and Delays Wound Healing: 100141– p.

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