HMGB1 is mechanistically essential in the development of experimental pulmonary hypertension.
Animals
Anti-Inflammatory Agents
/ pharmacology
Cell Hypoxia
/ drug effects
Cells, Cultured
Glycyrrhizic Acid
/ pharmacology
HMGB1 Protein
/ antagonists & inhibitors
Hypertension, Pulmonary
/ drug therapy
Male
Myocytes, Smooth Muscle
/ drug effects
Pulmonary Artery
/ drug effects
Rats
Rats, Sprague-Dawley
HMGB1
PI3K/Akt
TLR4
calcium
migration
pulmonary hypertension
Journal
American journal of physiology. Cell physiology
ISSN: 1522-1563
Titre abrégé: Am J Physiol Cell Physiol
Pays: United States
ID NLM: 100901225
Informations de publication
Date de publication:
01 02 2019
01 02 2019
Historique:
pubmed:
6
12
2018
medline:
15
11
2019
entrez:
6
12
2018
Statut:
ppublish
Résumé
Pulmonary hypertension (PH) is a mortal disease featuring pulmonary vascular constriction and remodeling, right heart failure, and eventual death. Several reports showed that high-mobility group box 1 (HMGB1) appears to be critical for the development of PH; the underlying mechanism, however, has not been revealed. Experiments in the present study demonstrated that HMGB1 levels were elevated in the lung tissue and blood plasma of rats after chronic hypoxia exposure and monocrotaline treatment. HMGB1 was originally located within the nucleus and translocated to the cytoplasm of pulmonary artery smooth muscle cells (PASMCs) upon hypoxia exposure, a process that appeared to be mediated by endogenous H
Identifiants
pubmed: 30517029
doi: 10.1152/ajpcell.00148.2018
doi:
Substances chimiques
Anti-Inflammatory Agents
0
HMGB1 Protein
0
Hbp1 protein, rat
0
Glycyrrhizic Acid
6FO62043WK
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
C175-C185Commentaires et corrections
Type : ErratumIn