Document Detail


Role of capacitative Ca2+ entry in bronchial contraction and remodeling.
MedLine Citation:
PMID:  11896026     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Asthma is characterized by airway inflammation, bronchial hyperresponsiveness, and airway obstruction by bronchospasm and bronchial wall thickening due to smooth muscle hypertrophy. A rise in cytosolic free Ca2+ concentration ([Ca2+]cyt) may serve as a shared signal transduction element that causes bronchial constriction and bronchial wall thickening in asthma. In this study, we examined whether capacitative Ca2+ entry (CCE) induced by depletion of intracellular Ca2+ stores was involved in agonist-mediated bronchial constriction and bronchial smooth muscle cell (BSMC) proliferation. In isolated bronchial rings, acetylcholine (ACh) induced a transient contraction in the absence of extracellular Ca2+ because of Ca2+ release from intracellular Ca2+ stores. Restoration of extracellular Ca2+ in the presence of atropine, an M-receptor blocker, induced a further contraction that was apparently caused by a rise in [Ca2+]cyt due to CCE. In single BSMC, amplitudes of the store depletion-activated currents (I(SOC)) and CCE were both enhanced when the cells proliferate, whereas chelation of extracellular Ca2+ with EGTA significantly inhibited the cell growth in the presence of serum. Furthermore, the mRNA expression of TRPC1, a transient receptor potential channel gene, was much greater in proliferating BSMC than in growth-arrested cells. Blockade of the store-operated Ca2+ channels by Ni2+ decreased I(SOC) and CCE and markedly attenuated BSMC proliferation. These results suggest that upregulated TRPC1 expression, increased I(SOC), enhanced CCE, and elevated [Ca2+]cyt may play important roles in mediating bronchial constriction and BSMC proliferation.
Authors:
Michele Sweeney; Sharon S McDaniel; Oleksandr Platoshyn; Shen Zhang; Ying Yu; Bethany R Lapp; Ying Zhao; Patricia A Thistlethwaite; Jason X-J Yuan
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't; Research Support, U.S. Gov't, P.H.S.    
Journal Detail:
Title:  Journal of applied physiology (Bethesda, Md. : 1985)     Volume:  92     ISSN:  8750-7587     ISO Abbreviation:  J. Appl. Physiol.     Publication Date:  2002 Apr 
Date Detail:
Created Date:  2002-03-15     Completed Date:  2002-07-08     Revised Date:  2013-09-26    
Medline Journal Info:
Nlm Unique ID:  8502536     Medline TA:  J Appl Physiol (1985)     Country:  United States    
Other Details:
Languages:  eng     Pagination:  1594-602     Citation Subset:  IM    
Affiliation:
Division of Pulmonary and Critical Care Medicine, Department of Medicine, School of Medicine, University of California, San Diego, California 92103, USA.
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MeSH Terms
Descriptor/Qualifier:
Acetylcholine / pharmacology
Animals
Asthma / metabolism
Atropine / pharmacology
Bronchi / cytology,  metabolism*
Bronchoconstriction / drug effects,  physiology
Bronchodilator Agents / pharmacology
Calcium / metabolism*
Calcium Channels / genetics,  metabolism
Calcium-Transporting ATPases / antagonists & inhibitors,  metabolism
Cell Division / physiology
Cells, Cultured
Enzyme Inhibitors / pharmacology
Gene Expression / physiology
Humans
Indoles / pharmacology
Muscle, Smooth / cytology,  metabolism*
Nickel / pharmacology
RNA, Messenger / analysis
Rats
Rats, Sprague-Dawley
Sarcoplasmic Reticulum Calcium-Transporting ATPases
TRPC Cation Channels
Grant Support
ID/Acronym/Agency:
HL-54043/HL/NHLBI NIH HHS; HL-64945/HL/NHLBI NIH HHS; HL-66012/HL/NHLBI NIH HHS; HL-69758/HL/NHLBI NIH HHS
Chemical
Reg. No./Substance:
0/Bronchodilator Agents; 0/Calcium Channels; 0/Enzyme Inhibitors; 0/Indoles; 0/RNA, Messenger; 0/TRPC Cation Channels; 0/transient receptor potential cation channel, subfamily C, member 1; 51-55-8/Atropine; 51-84-3/Acetylcholine; 7440-02-0/Nickel; 7440-70-2/Calcium; EC 3.6.3.8/Calcium-Transporting ATPases; EC 3.6.3.8/Sarcoplasmic Reticulum Calcium-Transporting ATPases; X9TLY4580Z/cyclopiazonic acid

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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