資料載入中.....
|
請使用永久網址來引用或連結此文件:
http://ir.cmu.edu.tw/ir/handle/310903500/29250
|
| 題名: | Nonassociation of interleukin 4 intron 3 and 590 promoter polymorphisms with bronchopulmonary dysplasia for ventilated preterm infants |
| 作者: | Lin, HC;Su, BH;Chang, JS;Hsu, CM;Tsai, CH;Tsai, FJ |
| 貢獻者: | 附設醫院兒科部;China Med Univ Hosp, Dept Pediat, Taichung 404, Taiwan;China Med Univ Hosp, Dept Med Genet, Taichung 404, Taiwan;Taichung Healthcare & Management Univ, Taichung, Taiwan |
| 日期: | 2005 |
| 上傳時間: | 2010-09-24 14:28:52 (UTC+8) |
| 出版者: | KARGER |
| 摘要: | Phenylarsine oxide (PAO), a trivalent arsenical compound, stimulated [Ca2+](i) elevation in rat neutrophils in a Ca2+-Containing medium but caused no appreciable response in a Ca2+-free medium. PAO also induced external Mn2+ entry, which was inhibited by N-acetyl-L-cysteine (NAC), but failed to elicit any appreciable Ba2+ and Sr2+ entry. Pretreatment of neutrophils with thiol-reducing agents including dithiothreitol (DTT), NAC, 2,3-dimercapto-1-propanol (DMP), 2,3-dimercaptopropane-1-sulfonic acid (DMPS) and tris-(2-carboxyethyl)phosphine (TCEP), all greatly inhibited PAO-induced [Ca2+](i) elevation. Addition of Ni2+ or La3+ followed by PAO stimulation also attenuated the Ca2+ signals in a concentration-dependent manner. PAO had no significant effect on the production of reactive oxygen intermediates (ROI) and nitric oxide (NO) nor did it decrease cellular low molecular weight thiols levels. PAO-induced [Ca2+](i) elevation was significantly inhibited by 1-[6-[17 beta-3-methoxyestra-1,3,5(10)-trien-17-yl]amino]hexyl]-1H-pyrrole-2,5-dione (U-73122), the inhibitor of phospholipase C-coupled processes, genistein, a general tyrosine kinase inhibitor, phorbol 12-myristate 13-acetate (PMA), a protein kinase C (PKC) activator, calyculin A, a cortical actin stabilizer, 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one (LY 294002), a phosphoinositide 3-kinase inhibitor, 1-[beta-[3-(4-methoxyphenyl)propoxyl-4-methoxyphenethyl]-1H-imidazole (SKF-96365), and cis-N-(2-phenylcyclopentyl)azacyclotridec-1-en-2-amine (MDL-12,330A), the blockers of receptor-gated and store-operated Ca2+ channels, whereas there was no appreciable effect exerted by aristolochic acid, a phospholipase A(2) inhibitor, 7-nitroindazole and N-(3-aminomethyl)benzylacetamidine (1400W), the blockers of NO synthase, and by suspension in a Na+-deprived medium. In contrast, 2-aminoethoxydiphenyl borane (2-APB), the blocker of IP3 receptor and Ca2+ influx, enhanced the PAO-induced response. PAO had no effect on the plasma membrane Ca2+-ATPase (PMCA) activity in the pharmacological isolated nentrophil preparation and the neutrophil membrane fractions. These results indicate that PAO stimulates [Ca2+](i) rise in rat neutrophils mainly through the oxidation of vicinal thiol groups on the cell surface membrane to activation of a non-store operated Ca2+ entry (non-SOCE) without affecting the activity of PMCA and the plasmalernmal Na+/Ca2+, exchanger. (c) 2005 Elsevier Inc. All rights reserved. |
| 關聯: | BIOLOGY OF THE NEONATE 87(3):181-186 |
| 顯示於類別: | [台中附設醫院] 期刊論文
|
在CMUR中所有的資料項目都受到原著作權保護.
|
