Hyo-Jong Lee" /> Min Wook Shin" /> " /> Hyo-Jong Lee, Bum Ju Ahn, Min Wook Shin, Jeong-Hyun Choi, and Kyu-Won Kim*" /> Hyo-Jong Lee, Bum Ju Ahn, Min Wook Shin, Jeong-Hyun Choi, and Kyu-Won Kim*. Mol. Cells 2010;29:223-7. https://doi.org/10.1007/s10059-010-0043-x">
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Mol. Cells 2010; 29(3): 223-227

Published online March 31, 2010

https://doi.org/10.1007/s10059-010-0043-x

© The Korean Society for Molecular and Cellular Biology

Ninjurin1: a Potential Adhesion Molecule and Its Role in Inflammation and Tissue Remodeling

Hyo-Jong Lee1, Bum Ju Ahn1, Min Wook Shin1, Jeong-Hyun Choi1, and Kyu-Won Kim1,2,*

1NeuroVascular Coordination Research Center, Research Institute of Pharmaceutical Sciences, College of Pharmacy, Seoul National University, Seoul 151-742, Korea, 2Department of Molecular Medicine and Biopharmaceutical Sciences, Graduate School of Convergence Science and Technology, Seoul National University, Seoul 151-742, Korea

Correspondence to : *Correspondence: qwonkim@plaza.snu.ac.kr

Received: January 4, 2010; Accepted: January 7, 2010

Abstract

Nerve injury induced protein 1, Ninj1 (Ninjurin1) is a cell surface protein that is induced by nerve injury and pro-motes axonal growth in the peripheral nervous system. However, the function of Ninj1 in the vascular system and central nervous system (CNS) is incompletely understood. Here we review recent studies that have shed further light on the role and regulation of Ninj1 in vascular remodeling and inflammation. Increasing evi-dence suggests that Ninj1 mediates cell communication and enhances the entry, migration, and activity of leukocytes such as monocytes and macrophages in developmental processes and inflammatory responses. Moreover, our recent studies show that Ninj1 regulates close interaction between leukocytes and vascular endothelial cells in vascular remodeling and inflamed CNS. Additionally, Ninj1 enhances the apoptosis-inducing activity of leukocytes and is cleaved by MMPs, resulting in loss of adhesion during tissue remodeling. The collective data described here show that Ninj1 is required for the entry, adhesion, activation, and movement of leukocytes during tissue remodeling and might be a potential therapeutic target to regulate the adhesion and trafficking of leukocytes in inflammation and leukocyte-mediated diseases such as multiple sclerosis, diabetic retinopathy, and neuropathy.

Keywords adhesion, cell-cell interaction, endothelial cells, ENT domain, inflammation, leukocyte, MMPs, Ninj1, tissue remodeling

Article

Minireview

Mol. Cells 2010; 29(3): 223-227

Published online March 31, 2010 https://doi.org/10.1007/s10059-010-0043-x

Copyright © The Korean Society for Molecular and Cellular Biology.

Ninjurin1: a Potential Adhesion Molecule and Its Role in Inflammation and Tissue Remodeling

Hyo-Jong Lee1, Bum Ju Ahn1, Min Wook Shin1, Jeong-Hyun Choi1, and Kyu-Won Kim1,2,*

1NeuroVascular Coordination Research Center, Research Institute of Pharmaceutical Sciences, College of Pharmacy, Seoul National University, Seoul 151-742, Korea, 2Department of Molecular Medicine and Biopharmaceutical Sciences, Graduate School of Convergence Science and Technology, Seoul National University, Seoul 151-742, Korea

Correspondence to:*Correspondence: qwonkim@plaza.snu.ac.kr

Received: January 4, 2010; Accepted: January 7, 2010

Abstract

Nerve injury induced protein 1, Ninj1 (Ninjurin1) is a cell surface protein that is induced by nerve injury and pro-motes axonal growth in the peripheral nervous system. However, the function of Ninj1 in the vascular system and central nervous system (CNS) is incompletely understood. Here we review recent studies that have shed further light on the role and regulation of Ninj1 in vascular remodeling and inflammation. Increasing evi-dence suggests that Ninj1 mediates cell communication and enhances the entry, migration, and activity of leukocytes such as monocytes and macrophages in developmental processes and inflammatory responses. Moreover, our recent studies show that Ninj1 regulates close interaction between leukocytes and vascular endothelial cells in vascular remodeling and inflamed CNS. Additionally, Ninj1 enhances the apoptosis-inducing activity of leukocytes and is cleaved by MMPs, resulting in loss of adhesion during tissue remodeling. The collective data described here show that Ninj1 is required for the entry, adhesion, activation, and movement of leukocytes during tissue remodeling and might be a potential therapeutic target to regulate the adhesion and trafficking of leukocytes in inflammation and leukocyte-mediated diseases such as multiple sclerosis, diabetic retinopathy, and neuropathy.

Keywords: adhesion, cell-cell interaction, endothelial cells, ENT domain, inflammation, leukocyte, MMPs, Ninj1, tissue remodeling

Mol. Cells
Aug 31, 2022 Vol.45 No.8, pp. 513~602
COVER PICTURE
Cryo-EM structure of human porphyrin transporter ABCB6 (main figure) shows that binding of hemin (inset, magenta) in concert with two glutathione molecules (cyan) primes ABCB6 for high ATP turnover (Kim et al., pp. 575-587).

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