Cleaved endocan acts as a biologic competitor of endocan in the control of ICAM-1-dependent leukocyte diapedesis.
Cell Adhesion
/ physiology
Chemotaxis, Leukocyte
/ physiology
Humans
Intercellular Adhesion Molecule-1
/ metabolism
Lymphocyte Function-Associated Antigen-1
/ metabolism
Neoplasm Proteins
/ metabolism
Proteoglycans
/ metabolism
T-Lymphocytes
/ metabolism
Transendothelial and Transepithelial Migration
/ physiology
acute lung injury
cleaved endocan
endocan
inflammation
leukocyte diapedesis
p14
Journal
Journal of leukocyte biology
ISSN: 1938-3673
Titre abrégé: J Leukoc Biol
Pays: England
ID NLM: 8405628
Informations de publication
Date de publication:
05 2020
05 2020
Historique:
received:
15
11
2019
revised:
10
03
2020
accepted:
11
03
2020
pubmed:
10
4
2020
medline:
5
11
2020
entrez:
10
4
2020
Statut:
ppublish
Résumé
Dysregulated leukocyte diapedesis is a major contributor to acute severe inflammatory states like sepsis and acute respiratory distress syndrome, which are common conditions in critically ill subjects. Endocan is a circulating proteoglycan that binds to the leukocyte integrin LFA-1 and blocks its interaction with its endothelial ligand ICAM-1, subsequently leading to the inhibition of leukocyte recruitment. Recent data have highlighted the hypothetic role of p14, endocan's major catabolite found in the bloodstream of septic patients, as a potential antagonist of endocan, thus participating in the regulation of acute inflammation. We hereby characterize the role of p14 as a biologic competitor of endocan, through assessment of its molecular interactions with LFA-1, endocan, and ICAM-1, as well as its effects on human leukocyte trafficking. Using immunodetection assay, we report that p14 can bind to LFA-1, thus inhibiting the interaction between LFA-1 and endocan, which in turn leads to the restoration of the ICAM-1/LFA-1 interaction. In primary human T cells trafficking assays, we underline the absence of effect of p14 on ICAM-1-dependent adhesion and migration, as well as on transendothelial migration. However, in those models, p14 reverses the antimigratory effect of endocan. To conclude, our study supports the hypothesis of an antagonistic role of p14 versus endocan in its effect on the LFA-1/ICAM-1-dependent human leukocyte recruitment.
Identifiants
pubmed: 32272492
doi: 10.1002/JLB.3AB0320-612RR
doi:
Substances chimiques
ESM1 protein, human
0
ICAM1 protein, human
0
Lymphocyte Function-Associated Antigen-1
0
Neoplasm Proteins
0
Proteoglycans
0
Intercellular Adhesion Molecule-1
126547-89-5
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
833-841Informations de copyright
©2020 Society for Leukocyte Biology.
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