TRPC channels mediated calcium entry is required for proliferation of human airway smooth muscle cells induced by nicotine-nAChR.
Aged
Calcium
/ metabolism
Calcium Signaling
/ drug effects
Cell Proliferation
/ drug effects
Female
Gene Expression Regulation
/ drug effects
Humans
Male
Middle Aged
Myocytes, Smooth Muscle
/ metabolism
Nicotine
/ pharmacology
Pulmonary Disease, Chronic Obstructive
/ metabolism
Receptors, Nicotinic
/ biosynthesis
Respiratory System
/ metabolism
TRPC Cation Channels
/ biosynthesis
Aortic smooth muscle cells
Calcium
Chronic obstructive pulmonary disease
Nicotinic acetylcholine receptor
Transient receptor potential canonical
Journal
Biochimie
ISSN: 1638-6183
Titre abrégé: Biochimie
Pays: France
ID NLM: 1264604
Informations de publication
Date de publication:
Mar 2019
Mar 2019
Historique:
received:
17
09
2018
accepted:
09
12
2018
pubmed:
15
12
2018
medline:
28
2
2019
entrez:
15
12
2018
Statut:
ppublish
Résumé
The present study was designed to explore the role of transient receptor potential canonical 3 (TRPC3) in nicotine-induced chronic obstructive pulmonary disease (COPD) and its underlying mechanism. In this study, the expression and localization of α5 nicotinic acetylcholine receptor (α5-nAchR) in lung tissues were determined by western blotting and immunohistochemistry. The quantitative real-time PCR (qRT-PCR) analysis was performed to examine the mRNA expression levels of α5-nAchR and TRPC3 in human airway smooth muscle cells (HASMCs). Cell viability was assessed by CCK-8 assay. Proliferation was detected by cell counting and EdU immunofluorescent staining. Fluorescence calcium imaging was carried out to measure cytosolic Ca
Identifiants
pubmed: 30550855
pii: S0300-9084(18)30349-3
doi: 10.1016/j.biochi.2018.12.004
pii:
doi:
Substances chimiques
Receptors, Nicotinic
0
TRPC Cation Channels
0
TRPC3 cation channel
0
nicotinic receptor alpha5 subunit, human
0
Nicotine
6M3C89ZY6R
Calcium
SY7Q814VUP
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Pagination
139-148Informations de copyright
Copyright © 2018. Published by Elsevier B.V.