Evidence map›Paper›PMID 24917672›Full record

ArticleThe Journal of biological chemistry2014

Ninjurin1 enhances the basal motility and transendothelial migration of immune cells by inducing protrusive membrane dynamics.

Bum Ju Ahn, Hoang Le, Min Wook Shin, Sung-Jin Bae, Eun Ji Lee, Sung Yi Lee, Ju Hee Yang, Hee-Jun Wee, Jong-Ho Cha, Ji Hae Seo and 10 more

Open access · hybridAbstract read
In one paragraph

Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.

0numbers the graph read from it
0cells of the map it votes in
23citing papers in PubMed
0.8field-weighted citation impact, top 29% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

23 citing papers in PubMed, 40 citations in OpenAlex.

  1. NINJ1: implications for plasma membrane rupture and disease.Biochemical Society transactions · 2026
    Review
  2. The role of NINJ1 in diseases.Cell death discovery · 2026
    Review
  3. Review
  4. Review
  5. NINJ1 impairs the anti-inflammatory function of hUC-MSCs with synergistic IFN-γ and TNF-α stimulation.Chinese journal of traumatology = Zhonghua chuang shang za zhi · 2025
    Article
  6. Review
  7. Article
  8. A guide to cell death pathways.Nature reviews. Molecular cell biology · 2024
    Review
  9. Article
  10. Review
  11. Article
  12. Role of NINJ1 in Gout Flare and Potential as a Drug Target.Journal of inflammation research · 2022
    Article
  13. Pyroptosis in spinal cord injury.Frontiers in cellular neuroscience · 2022
    Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Article
  19. Article
  20. Article
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

20 authors at 5 institutions in 2 countries.

Bum Ju AhnFrom the SNU-Harvard NeuroVascular Protection Research Center, College of Pharmacy and Research Institute of Pharmaceutical Sciences, Seoul National University, Seoul 151-742, Korea.
Hoang LeFrom the SNU-Harvard NeuroVascular Protection Research Center, College of Pharmacy and Research Institute of Pharmaceutical Sciences, Seoul National University, Seoul 151-742, Korea.
Min Wook ShinFrom the SNU-Harvard NeuroVascular Protection Research Center, College of Pharmacy and Research Institute of Pharmaceutical Sciences, Seoul National University, Seoul 151-742, Korea.
Sung-Jin BaeFrom the SNU-Harvard NeuroVascular Protection Research Center, College of Pharmacy and Research Institute of Pharmaceutical Sciences, Seoul National University, Seoul 151-742, Korea.
Eun Ji LeeFrom the SNU-Harvard NeuroVascular Protection Research Center, College of Pharmacy and Research Institute of Pharmaceutical Sciences, Seoul National University, Seoul 151-742, Korea.
Sung Yi LeeFrom the SNU-Harvard NeuroVascular Protection Research Center, College of Pharmacy and Research Institute of Pharmaceutical Sciences, Seoul National University, Seoul 151-742, Korea.
Ju Hee YangFrom the SNU-Harvard NeuroVascular Protection Research Center, College of Pharmacy and Research Institute of Pharmaceutical Sciences, Seoul National University, Seoul 151-742, Korea.
Hee-Jun WeeFrom the SNU-Harvard NeuroVascular Protection Research Center, College of Pharmacy and Research Institute of Pharmaceutical Sciences, Seoul National University, Seoul 151-742, Korea.
Jong-Ho ChaFrom the SNU-Harvard NeuroVascular Protection Research Center, College of Pharmacy and Research Institute of Pharmaceutical Sciences, Seoul National University, Seoul 151-742, Korea.
Ji Hae SeoFrom the SNU-Harvard NeuroVascular Protection Research Center, College of Pharmacy and Research Institute of Pharmaceutical Sciences, Seoul National University, Seoul 151-742, Korea.
Hye Shin LeeFrom the SNU-Harvard NeuroVascular Protection Research Center, College of Pharmacy and Research Institute of Pharmaceutical Sciences, Seoul National University, Seoul 151-742, Korea.
Hyo-Jong Leethe College of Pharmacy, Inje University, Gimhae 621-749, Korea.
Ken Araithe Neuroprotection Research Laboratory, Departments of Radiology and Neurology, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts 02114.
Eng H Lothe Neuroprotection Research Laboratory, Departments of Radiology and Neurology, Massachusetts General Hospital and Harvard Medical School, Boston, Massachusetts 02114.
Sejin Jeonthe Department of Life Science and GT5 Program, Ewha Womans University, Seodaemoon-gu, Seoul 120-750, Korea, and.
Goo Taeg Ohthe Department of Life Science and GT5 Program, Ewha Womans University, Seodaemoon-gu, Seoul 120-750, Korea, and.
Woo Jean Kimthe National Research Center for Sexual Medicine and Department of Urology, Inha University School of Medicine, Incheon 402-751, Korea.
Ji-Kan Ryuthe National Research Center for Sexual Medicine and Department of Urology, Inha University School of Medicine, Incheon 402-751, Korea.
Jun-Kyu Suhthe National Research Center for Sexual Medicine and Department of Urology, Inha University School of Medicine, Incheon 402-751, Korea.
Kyu-Won KimFrom the SNU-Harvard NeuroVascular Protection Research Center, College of Pharmacy and Research Institute of Pharmaceutical Sciences, Seoul National University, Seoul 151-742, Korea, the Department of Molecular Medicine and Biopharmaceutical Sciences, Graduate School of Convergence Science and Technology, and College of Medicine or College of Pharmacy, Seoul National University, Seoul 151-742, Korea, qwonkim@snu.ac.kr.
Seoul National University · KRInha University · KREwha Womans University · KRHarvard University · USInje University · KR

Funding

Targeting ROCK for Neurogliovascular Plasticity & Remodeling After StrokeP01NS055104 · NINDS · MASSACHUSETTS GENERAL HOSPITAL · PI LO, ENG H. · 2007 to 2018
$13.3M
Biphasic mechanisms of injury and repair in stroke therapyR37NS037074 · NINDS · MASSACHUSETTS GENERAL HOSPITAL · PI LO, ENG H. · 2008 to 2015
$3.2M
NINDS NIH HHS P01 NS055104NINDS NIH HHS P01-NS55104NINDS NIH HHS R37 NS037074NINDS NIH HHS R37-NS37074
6 · The paper itself

Abstract

Ninjurin1 is involved in the pathogenesis of experimental autoimmune encephalomyelitis, an animal model of multiple sclerosis, by mediating leukocyte extravasation, a process that depends on homotypic binding. However, the precise regulatory mechanisms of Ninjurin1 during inflammation are largely undefined. We therefore examined the pro-migratory function of Ninjurin1 and its regulatory mechanisms in macrophages. Interestingly, Ninjurin1-deficient bone marrow-derived macrophages exhibited reduced membrane protrusion formation and dynamics, resulting in the impairment of cell motility. Furthermore, exogenous Ninjurin1 was distributed at the membrane of filopodial structures in Raw264.7 macrophage cells. In Raw264.7 cells, RNA interference of Ninjurin1 reduced the number of filopodial projections, whereas overexpression of Ninjurin1 facilitated their formation and thus promoted cell motility. Ninjurin1-induced filopodial protrusion formation required the activation of Rac1. In Raw264.7 cells penetrating an MBEC4 endothelial cell monolayer, Ninjurin1 was localized to the membrane of protrusions and promoted their formation, suggesting that Ninjurin1-induced protrusive activity contributed to transendothelial migration. Taking these data together, we conclude that Ninjurin1 enhances macrophage motility and consequent extravasation of immune cells through the regulation of protrusive membrane dynamics. We expect these findings to provide insight into the understanding of immune responses mediated by Ninjurin1.

Indexed as

AnimalsCell AdhesionCell Adhesion Molecules, NeuronalCell LineCell MembraneCell MovementCells, CulturedEndothelial CellsGene Knockdown TechniquesInflammationMacrophagesMiceMice, Inbred C57BLMice, KnockoutModels, BiologicalNerve Growth FactorsCell Adhesion Molecules, NeuronalNerve Growth FactorsNeuropeptidesNinj1 protein, mouserac1 GTP-Binding ProteinRac1 protein, mouseCell MigrationCell MotilityFilopodiaInflammationMacrophageNinjurin1Ras-related C3 Botulinum Toxin Substrate 1 (Rac1)Transendothelial Migration

Identifiers

PMID24917672
PMCPMC4139210
OpenAlexW2043409184

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.