alpha1A-adrenoceptor is involved in norepinephrine-induced proliferation of pulmonary artery smooth muscle cells via CaMKII signaling.
Animals
Calcium-Calmodulin-Dependent Protein Kinase Type 2
/ genetics
Cell Hypoxia
/ genetics
Cell Movement
/ drug effects
Cell Proliferation
/ drug effects
Disease Models, Animal
Humans
Myocytes, Smooth Muscle
Norepinephrine
/ adverse effects
Phosphorylation
Pulmonary Arterial Hypertension
/ chemically induced
Pulmonary Artery
/ drug effects
Rats
Receptors, Adrenergic, alpha-1
/ genetics
Signal Transduction
/ drug effects
Sympathetic Nervous System
/ drug effects
alpha1A-adrenoceptor (α1A-AR)
calcium/calmodulin(CaM)-dependent protein kinase type II (CaMKII) pathway
norepinephrine (NE)
proliferation of pulmonary artery smooth muscle cells (PASMCs)
pulmonary arterial hypertension (PAH)
Journal
Journal of cellular biochemistry
ISSN: 1097-4644
Titre abrégé: J Cell Biochem
Pays: United States
ID NLM: 8205768
Informations de publication
Date de publication:
06 2019
06 2019
Historique:
received:
27
07
2018
accepted:
15
11
2018
pubmed:
7
12
2018
medline:
18
7
2020
entrez:
7
12
2018
Statut:
ppublish
Résumé
Pulmonary arterial hypertension (PAH) is a progressive disease of the pulmonary vasculature characterized by excessive proliferation of pulmonary artery smooth muscle cells (PASMCs). Some studies have demonstrated the sympathetic nervous system is activated in PAH and norepinephrine (NE) released is closely linked with its activation. However, the subtypes of adrenoreceptor (AR) and the downstream molecular cascades which are involved in the proliferation of PASMCs are still unclear. In this study, adult male Wistar rats were exposed to chronic hypoxia and PASMCs were cultured in hypoxic condition. Significant upregulation of α
Substances chimiques
Receptors, Adrenergic, alpha-1
0
Calcium-Calmodulin-Dependent Protein Kinase Type 2
EC 2.7.11.17
Norepinephrine
X4W3ENH1CV
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Pagination
9345-9355Informations de copyright
© 2018 Wiley Periodicals, Inc.