title: Ninjurin1: a potential adhesion molecule and its role in inflammation and tissue remodeling.
abstract: Nerve injury induced protein 1, Ninj1 (Ninjurin1) is a cell surface protein that is induced by nerve injury and promotes 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 evidence 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.
authors.affiliation: NeuroVascular Coordination Research Center, Research Institute of Pharmaceutical Sciences, College of Pharmacy, Seoul National University, Seoul, 151-742, Korea.
authors.forename: Hyo-Jong
authors.initials: HJ
authors.lastname: Lee
authors.forename: Bum Ju
authors.initials: BJ
authors.lastname: Ahn
authors.forename: Min Wook
authors.initials: MW
authors.lastname: Shin
authors.forename: Jeong-Hyun
authors.initials: JH
authors.lastname: Choi
authors.forename: Kyu-Won
authors.initials: KW
authors.lastname: Kim
mesh_terms: D000818:Animals; D017209:Apoptosis / Q000502:physiology*; D001327:Autoimmune Diseases / Q000276:immunology / Q000503:physiopathology; D001808:Blood Vessels / Q000166:cytology; D002448:Cell Adhesion / Q000502:physiology*; D015816:Cell Adhesion Molecules, Neuronal / Q000737:chemistry / Q000502:physiology*; D002450:Cell Communication / Q000502:physiology; D002465:Cell Movement / Q000502:physiology; D016503:Drug Delivery Systems; D042783:Endothelial Cells / Q000166:cytology; D006801:Humans; D007249:Inflammation / Q000188:drug therapy / Q000503:physiopathology*; D007962:Leukocytes / Q000166:cytology; D020782:Matrix Metalloproteinases / Q000502:physiology; D009414:Nerve Growth Factors / Q000737:chemistry / Q000502:physiology*; D009416:Nerve Regeneration / Q000502:physiology*; D059348:Peripheral Nerve Injuries; D017434:Protein Structure, Tertiary; D013329:Structure-Activity Relationship
chemical_list: D015816:Cell Adhesion Molecules, Neuronal; D009414:Nerve Growth Factors; D020782:Matrix Metalloproteinases