Role of sarcoplasmic reticulum Ca 2+ content in Ca 2+ entry of bovine airway smooth muscle cells

2003 ◽  
Vol 368 (4) ◽  
pp. 277-283 ◽  
Author(s):  
Blanca Baz�n-Perkins ◽  
Edgar Flores-Soto ◽  
Carlos Barajas-L�pez ◽  
Luis M. Monta�o
Keyword(s):  
Smooth Muscle ◽  
Sarcoplasmic Reticulum ◽  
Smooth Muscle Cells ◽  
Airway Smooth Muscle ◽  
Muscle Cells ◽  
Airway Smooth Muscle Cells

Sarcoplasmic Reticulum Ca2+ Depletion by Caffeine and Changes of [Ca2+]i During Refilling in Bovine Airway Smooth Muscle Cells

2000 ◽  
Vol 31 (6) ◽  
pp. 558-563 ◽  
Author(s):  
Blanca Bazán-Perkins ◽  
Edgar Sánchez-Guerrero ◽  
Verónica Carbajal ◽  
Carlos Barajas-López ◽  
Luis M. Montaño
Keyword(s):  
Smooth Muscle ◽  
Sarcoplasmic Reticulum ◽  
Smooth Muscle Cells ◽  
Airway Smooth Muscle ◽  
Muscle Cells ◽  
Airway Smooth Muscle Cells

Cyclic mechanical strain‐induced proliferation and migration of human airway smooth muscle cells: role of EMMPRIN and MMPs

2005 ◽  
Vol 19 (11) ◽  
pp. 1507-1509 ◽  
Author(s):  
Nadia A. Hasaneen ◽  
Stanley Zucker ◽  
Jian Cao ◽  
Christian Chiarelli ◽  
Reynold A. Panettieri ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Airway Smooth Muscle ◽  
Mechanical Strain ◽  
Muscle Cells ◽  
Airway Smooth Muscle Cells ◽  
Human Airway Smooth Muscle ◽  
And Migration ◽  
Proliferation And Migration

scholarly journals Mitochondria depletion abolishes agonist-induced Ca2+ plateau in airway smooth muscle cells: potential role of H2O2

2010 ◽  
Vol 298 (2) ◽  
pp. L178-L188 ◽  
Author(s):  
Taoxiang Chen ◽  
Liping Zhu ◽  
Tao Wang ◽  
Hong Ye ◽  
Kewu Huang ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Airway Smooth Muscle ◽  
Potential Role ◽  
Reactive Oxygen Species Generation ◽  
Muscle Cells ◽  
Airway Smooth Muscle Cells ◽  
Cellular Energy ◽  
Dependent Mechanism

The mechanisms by which mitochondria regulate the sustained phase of agonist-induced responses in cytosolic Ca2+ concentration as an independent organelle in whole is not clear. By exposing to ethidium bromide and supplying pyruvate and uridine, we established mitochondrial DNA (mtDNA)-depleted rat airway smooth muscle cells (RASMCs) with maintained cellular energy. Upon an exposure to 2 μM histamine, [Ca2+]i in control RASMCs increased to a peak followed by a plateau above baseline, whereas [Ca2+]i in mtDNA-depleted RASMCs jumped to a peak and then declined to baseline without any plateau. mtDNA depletion apparently attenuated intracellular reactive oxygen species generation induced by histamine. By coexposure to 2 μM histamine and 0.1 μM exogenous H2O2, which did not affect [Ca2+]i by itself, the above difference in [Ca2+]i kinetics in mtDNA-depleted RASMCs was reversed. Intracellular H2O2 decomposition abolishes histamine-induced sustained elevation in [Ca2+]i in RASMCs. Thus, mitochondria regulate agonist-induced sustained [Ca2+]i elevation by a H2O2-dependent mechanism.

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