期刊
AMERICAN JOURNAL OF PHYSIOLOGY-LUNG CELLULAR AND MOLECULAR PHYSIOLOGY
卷 298, 期 2, 页码 L178-L188出版社
AMER PHYSIOLOGICAL SOC
DOI: 10.1152/ajplung.00134.2009
关键词
histamine; calcium; reactive oxygen species
资金
- National Natural Science Foundation of China [30470758, 30670926, 30770943, 30871121, 30700340]
- Ministry of Health of China
Chen T, Zhu L, Wang T, Ye H, Huang K, Hu Q. Mitochondria depletion abolishes agonist-induced Ca2+ plateau in airway smooth muscle cells: potential role of H2O2. Am J Physiol Lung Cell Mol Physiol 298: L178-L188, 2010. First published November 20, 2009; doi: 10.1152/ajplung.00134.2009.-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 mu M 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 mu M histamine and 0.1 mu M 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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