Reactive oxygen and nitrogen intermediates increase transforming growth factor-beta1 release from human epithelial alveolar cells through two different mechanisms.
Reactive oxygen and nitrogen intermediates increase transforming growth factor-beta1 release from human epithelial alveolar cells through two different mechanisms.
复制标题
活性氧和氮中间体通过两种不同的机制增加人上皮肺泡细胞的转化生长因子-β1 释放。
DOI:
--
复制
发表时间:
1999
影响因子:
6.4
通讯作者:
L. Baud
中科院分区:
文献类型:
--
作者:
A. Bellocq;E. Azoulay;S. Marullo;Antoine Flahault;B. Fouqueray;C. Philippe;Jacques Cadranel;L. Baud
Transforming growth factor (TGF)-beta1 is a growth factor involved in the mechanisms of lung repair and fibrosis that follow inflammatory processes. We sought to examine the link between the generation of reactive oxygen intermediates (ROI) or reactive nitrogen intermediates (RNI) by inflammatory cells and the expression of TGF-beta1 by alveolar epithelial cells. Exposure of the A549 lung epithelial cell line to either an ROI generating system (xanthine and xanthine oxidase) or an RNI donor (S-nitroso-N-acetyl-penicillamine [SNAP]) promoted a time- and dose-dependent increase in TGF-beta1 release, as measured by a specific enzyme-linked immunosorbent assay. At the peak, the levels of TGF-beta1 were twice the control values. The induction of TGF-beta1 release by ROI was blunted by catalase and unaffected by superoxide dismutase, indicating the involvement of hydrogen peroxide. The response was also blunted by 5, 6-dichloro-1-beta-D-ribofuranosyl benzimidazole (DRB), a specific RNA polymerase II inhibitor, and accompanied by a corresponding increase in TGF-beta1 messenger RNA, as measured by quantitative/competitive reverse transcription polymerase chain reaction, suggesting the involvement of transcriptional mechanisms and possibly other downstream mechanisms. In contrast, RNI-induced TGF-beta1 release was unaffected by DRB and blunted by the protein synthesis inhibitor cycloheximide, suggesting the involvement of translational and post-translational mechanisms. This response required cyclic guanosine monophosphate (cGMP)- mediated processes because (1) immunoreactive cGMP accumulated in the culture medium of SNAP-treated cells; (2) SNAP-induced TGF-beta1 release was blunted by KT 5823, an inhibitor of cGMP-dependent protein kinase; and (3) similar increase in TGF-beta1 release was obtained by cell exposure to membrane-permeable dibutyryl-cGMP or to atrial natriuretic factor, a known agonist of particulate guanylate cyclase. These data suggest that in vitro exposure of human alveolar epithelial cells to ROI and RNI enhances TGF-beta1 release through different mechanisms. In vivo, this control may constitute a molecular link between inflammatory and fibrotic processes.
登录
查看更多内容
影响因子:
5.8
作者:
Q. Wang;S. Giri;D. Hyde;C. Li
通讯作者:
Q. Wang;S. Giri;D. Hyde;C. Li
DOI:
--
发表时间:
1981-09
期刊:
The Journal of pharmacology and experimental therapeutics
影响因子:
--
作者:
L. Ignarro;H. Lippton;J. Edwards;W. Baricos;A. Hyman;P. Kadowitz;C. A. Gruetter
通讯作者:
L. Ignarro;H. Lippton;J. Edwards;W. Baricos;A. Hyman;P. Kadowitz;C. A. Gruetter
DOI:
10.1073/pnas.88.15.6642
发表时间:
1991-08-01
影响因子:
11.1
作者:
BROEKELMANN, TJ;LIMPER, AH;MCDONALD, JA
通讯作者:
MCDONALD, JA
DOI:
10.1073/pnas.89.18.8626
发表时间:
1992-09-15
影响因子:
11.1
作者:
GADBOIS, DM;CRISSMAN, HA;BRADBURY, EM
通讯作者:
BRADBURY, EM
DOI:
--
发表时间:
1994
期刊:
The Journal of biological chemistry
影响因子:
--
作者:
Cazals,V;Mouhieddine,B;Maitre,B;LeBouc,Y;Chadelat,K;Brody,JS;Clement,A
通讯作者:
Clement,A