Cobalt Induces Hypoxia-Inducible Factor-1α Expression in Airway Smooth Muscle Cells by a Reactive Oxygen Species– and PI3K-Dependent Mechanism

2004 ◽  
Vol 31 (5) ◽  
pp. 544-551 ◽  
Author(s):  
Georgia Chachami ◽  
George Simos ◽  
Apostolia Hatziefthimiou ◽  
Sophia Bonanou ◽  
Paschalis-Adam Molyvdas ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Airway Smooth Muscle ◽  
Hypoxia Inducible Factor ◽  
Muscle Cells ◽  
Airway Smooth Muscle Cells ◽  
Oxygen Species ◽  
Hypoxia Inducible Factor 1Α ◽  
Dependent Mechanism

Reactive oxygen species induce a Ca2+-spark increase in sensitized murine airway smooth muscle cells

2013 ◽  
Vol 434 (3) ◽  
pp. 498-502 ◽  
Author(s):  
Qing-Rong Tuo ◽  
Yun-Fei Ma ◽  
Weiwei Chen ◽  
Xiao-Jing Luo ◽  
Jinhua Shen ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Smooth Muscle ◽  
Smooth Muscle Cells ◽  
Airway Smooth Muscle ◽  
Reactive Oxygen ◽  
Muscle Cells ◽  
Airway Smooth Muscle Cells ◽  
Oxygen Species

Exposure of differentiated airway smooth muscle cells to serum stimulates both induction of hypoxia-inducible factor-1α and airway responsiveness to ACh

2007 ◽  
Vol 293 (4) ◽  
pp. L913-L922 ◽  
Author(s):  
Georgia Chachami ◽  
Apostolia Hatziefthimiou ◽  
Panagiotis Liakos ◽  
Maria G. Ioannou ◽  
Georgios K. Koukoulis ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Smooth Muscle ◽  
Airway Smooth Muscle ◽  
Hypoxia Inducible Factor ◽  
Reactive Oxygen ◽  
Serum Starvation ◽  
Airway Smooth Muscle Cells ◽  
Oxygen Species ◽  
Phosphatidylinositol 3 Kinase ◽  
Phosphatidylinositol 3

Airway smooth muscle (ASM) cells are characterized by phenotypic plasticity and can switch between differentiated and proliferative phenotypes. In rabbit tracheal ASM cells that had been differentiated in vitro by serum starvation, readdition of FBS caused initiation of proliferation and induction of nuclear and transcriptionally active hypoxia-inducible factor (HIF)-1α. In addition, FBS stimulated the induction of HIF-1α by the hypoxia mimetic cobalt. Treatment with actinomycin D, cycloheximide, the phosphatidylinositol 3-kinase inhibitors LY-294002 and wortmannin or the reactive oxygen species scavenger diphenyleneiodonium inhibited the FBS-dependent induction of HIF-1α. These data indicate that, in differentiated ASM cells, FBS upregulates HIF-1α by a transcription-, translation-, phosphatidylinositol 3-kinase-, and reactive oxygen species-dependent mechanism. Interestingly, addition of FBS and cobalt also induced HIF-1α in organ cultures of rabbit trachea strips and synergistically increased their contractile response to ACh, suggesting that HIF-1α might be implicated in airway hypercontractility.

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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