The tight junction protein cingulin regulates the vascular response to burn injury in a mouse model.
Animals
Burns
/ genetics
Capillary Permeability
Disease Models, Animal
Edema
/ genetics
Endothelial Cells
/ metabolism
Leukocyte Rolling
Male
Membrane Proteins
/ deficiency
Mice, Inbred C57BL
Mice, Knockout
Microvessels
/ metabolism
Neovascularization, Physiologic
Signal Transduction
Skin
/ blood supply
Tight Junctions
/ genetics
Wound Healing
Angiogenesis
Burn injury
Cingulin
Edema
Mouse model
Tight junction
Vascular barrier
Vessel dilation
Wound healing
Journal
Microvascular research
ISSN: 1095-9319
Titre abrégé: Microvasc Res
Pays: United States
ID NLM: 0165035
Informations de publication
Date de publication:
11 2020
11 2020
Historique:
received:
26
06
2020
revised:
25
08
2020
accepted:
27
08
2020
pubmed:
3
9
2020
medline:
16
12
2020
entrez:
3
9
2020
Statut:
ppublish
Résumé
Edema formation due to the collapse of physiological barriers and the associated delayed healing process is still a central problem in the treatment of burn injuries. In healthy individuals, tight junctions form a barrier to fluid and small molecules. Cingulin is a cytoplasmic component of tight junctions and is involved in the regulation of the paracellular barrier. Endothelial specific cingulin knock-out mice provide new insight into the influence of tight junction proteins on edema formation and angiogenesis during wound healing. Knock-out mice lacking the head domain of cingulin in endothelial cells (Cgn
Identifiants
pubmed: 32877697
pii: S0026-2862(20)30127-8
doi: 10.1016/j.mvr.2020.104067
pii:
doi:
Substances chimiques
Cgn protein, mouse
0
Membrane Proteins
0
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
104067Informations de copyright
Copyright © 2020 The Author(s). Published by Elsevier Inc. All rights reserved.
Déclaration de conflit d'intérêts
Declaration of competing interest The authors have no competing interests.