Ninjurin1 deletion in neuron-glial antigen 2-positive pericytes prevents microvessel maturation and delays wound healing （Neuron-glial antigen 2 陽性周細胞におけるNinjurin1の欠損は微小血管の成熟化を抑制し創傷治癒を遅延させる）
著者
松尾, 梨沙
(Matsuo, Risa)
上位タイトル
JID innovations : skin science from molecules to population health.
Vol.2,
No.6
(2022.
7)
,p.100141-
識別番号
ISSN
2667-0267
DOI
10.1016/j.xjidi.2022.100141
その他
PMID:36262667
博士論文情報
学位授与番号
10107A582
学位授与年月日
2022-09-30
学位名
博士（医学）
学位授与機関
旭川医科大学
抄録
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.
