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Cited by 71Cell Adhesion Molecules ResearchNeuroinflammation and Neurodegeneration MechanismsInflammation biomarkers and pathways

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

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Lee, Hyo-Jong, Ahn, Bum Ju, Shin, Min Wook, Choi, Jeong-Hyun, Kim, Kyu-Won·2010·Molecules and Cells
DOI 10.1007/s10059-010-0043-x
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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.

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  • Early microglial changes included significant upregulation of gene sets involved in inflammatory processes, interferon response, Fc receptors, MHC class II components, and complement components.

    “Early changes included significant upregulation of gene sets involved in inflammatory processes (IL1B, CSF1R, STAB1, NINJ1, JAK3)61–65, interferon response (IRF1, IRF7, IFI16), Fc receptors (FCGR1A, FCGR1B, FCGR2A, FCGR3B), components of the class II major histocompatibility complex (MHC) (CD74, HLA-DRB5) and complement components (C1QA, C1QB) (Fig. 6d, top, red).”

    From Integrated multimodal cell atlas of Alzheimer’s disease (2024) · cites this paper as [64]

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Metadata

Authors
Lee, H.-J., Ahn, B. J., Shin, M. W., Choi, J.-H., & Kim, K.-W.
Affiliations
Seoul National University (KR)
Corresponding author
Kim, Kyu-Won
ORCID
Venue
Molecules and Cells
Publisher
Elsevier BV
Published
2010-03
Volume
29
Issue
3
Pages
223-228
ISSN
  • 0219-1032 (ISSN-L)
  • 1016-8478
DOI
10.1007/s10059-010-0043-x
OpenAlex
W1998192362
Cited by
71
References
2
Citations by year
2026: 5 · 2025: 8 · 2024: 10 · 2023: 5 · 2022: 13 · 2021: 2 · 2020: 3 · 2019: 4 · 2018: 2 · 2017: 1 · 2016: 3 · 2015: 5 · 2014: 1 · 2013: 2 · 2012: 5
FWCI
0.32
Type
journal article
Language
en
Open access
Licence
Locations
  • Molecules and Cells (publishedVersion, cc-by-nc-sa)
  • PubMed (publishedVersion)
Topics
  • Health Sciences › Medicine › Immunology and Allergy › Cell Adhesion Molecules Research
  • Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
  • Life Sciences › Immunology and Microbiology › Immunology › Inflammation biomarkers and pathways
Keywords
NINJ1, adhesion molecules, inflammation, tissue remodeling, vascular remodeling, leukocyte migration, monocytes, macrophages, leukocyte-endothelium interaction, apoptosis, multiple sclerosis, diabetic retinopathy, neuropathy, nerve injury
MeSH terms
Animals, Autoimmune Diseases, Blood Vessels, Cell Adhesion, Cell Communication, Cell Movement, Humans, Inflammation, Leukocytes, Nerve Growth Factors, Nerve Regeneration, Structure-Activity Relationship, Cell Adhesion Molecules, Neuronal, Drug Delivery Systems, Apoptosis, Protein Structure, Tertiary, Matrix Metalloproteinases, Endothelial Cells, Peripheral Nerve Injuries

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