Pharmacological blockage of ICAM-1 improves angiotensin II-induced cardiac remodeling by inhibiting adhesion of LFA-1
Angiotensin II
/ toxicity
Animals
Antibodies, Neutralizing
/ immunology
Cell Adhesion
Endothelium, Vascular
/ metabolism
Heart Failure
/ etiology
Human Umbilical Vein Endothelial Cells
/ metabolism
Humans
Intercellular Adhesion Molecule-1
/ blood
Lymphocyte Function-Associated Antigen-1
/ genetics
Macrophages
/ metabolism
Male
Mice
Mice, Inbred C57BL
Monocytes
/ metabolism
Myocardial Contraction
ICAM-1
adhesion
angiotensin II
cardiac remodeling
inflammation
macrophage
Journal
American journal of physiology. Heart and circulatory physiology
ISSN: 1522-1539
Titre abrégé: Am J Physiol Heart Circ Physiol
Pays: United States
ID NLM: 100901228
Informations de publication
Date de publication:
01 12 2019
01 12 2019
Historique:
pubmed:
16
11
2019
medline:
14
4
2020
entrez:
16
11
2019
Statut:
ppublish
Résumé
Intercellular adhesion molecule-1 (ICAM-1) is a member of an immunoglobulin-like superfamily of adhesion molecules that mediate leukocyte adhesion to vascular endothelium and are involved in several cardiovascular diseases, including ischemia-reperfusion injury, myocardial infarction, and atherosclerosis. However, the role of ICAM-1 in angiotensin II (ANG II)-induced cardiac remodeling in mice remains unclear. Wild-type mice were administered an IgG control or ICAM-1 neutralizing antibody (1 and 2 mg/mouse, respectively) and ANG II (1,000 ng·kg
Identifiants
pubmed: 31729904
doi: 10.1152/ajpheart.00566.2019
doi:
Substances chimiques
Antibodies, Neutralizing
0
Lymphocyte Function-Associated Antigen-1
0
Angiotensin II
11128-99-7
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