Thioredoxin prevents the development and progression of elastase-induced emphysema

被引:43
作者
Kinoshita, Takashi
Hoshino, Tomoaki [1 ]
Imaoka, Haruki
Ichiki, Hiroko
Okamoto, Masaki
Kawayama, Tomotaka
Yodoi, Junji
Kato, Seiya
Aizawa, Hisamichi
机构
[1] Kurume Univ, Sch Med, Dept Med, Div Respirol Neurol & Rheumatol, Kurume, Fukuoka 8300011, Japan
[2] Kyoto Univ, Inst Virus Res, Dept Biol Responses, Kyoto 6068507, Japan
[3] Univ Ryukyus, Grad Sch, Div Pathol & Cell Biol, Okinawa 9030215, Japan
[4] Univ Ryukyus, Fac Med, Okinawa 9030215, Japan
关键词
emphysema; oxidant stress; redox; thioredoxin; COPD;
D O I
10.1016/j.bbrc.2007.01.053
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 [生物化学与分子生物学]; 081704 [应用化学];
摘要
Thioredoxin I (TRX1) is a redox (reduction/oxidation) -active protein that scavenges reactive oxygen species. Here we examined whether endogenous or exogenous administration of TRX1 prevented the development and progression of elastase-induced pulmonary emphysema. Mice were treated with intratracheal elastase via microspray on day 0, and were given recombinant human TRX1 (rhTRX1) every other day from days -1 to 21. To determine the effects of TRX1 on the progression of established emphysema, mice were treated intratracheally with elastase on day 0, and rhTRX1 was administered from days 14 to 21. Histopathologic examination was performed on day 21. TRX1-transgenic but not transgene-negative mice demonstrated a decrease in the physiological indicators of elastase-induced emphysema. TRX1 administration from days -1 to 19 significantly decreased the signs of elastase-induced emphysema. Moreover, TRX1 administration beginning 14 days after elastase treatment significantly slowed the progression of emphysema. TRX1 may be of clinical benefit for the treatment of COPD. (c) 2007 Elsevier lnc. All rights reserved.
引用
收藏
页码:712 / 719
页数:8
相关论文
共 24 条
[1]
Signalling pathways of the TNF superfamily: A double-edged sword [J].
Aggarwal, BB .
NATURE REVIEWS IMMUNOLOGY, 2003, 3 (09) :745-756
[2]
Aoshiba K, 2001, AM J PHYSIOL-LUNG C, V281, pL556
[3]
Alveolar wall apoptosis causes lung destruction and emphysematous changes [J].
Aoshiba, K ;
Yokohori, N ;
Nagai, A .
AMERICAN JOURNAL OF RESPIRATORY CELL AND MOLECULAR BIOLOGY, 2003, 28 (05) :555-562
[4]
Randomised, double blind, placebo controlled study of fluticasone propionate in patients with moderate to severe chronic obstructive pulmonary disease: the ISOLDE trial [J].
Burge, PS ;
Calverley, PMA ;
Jones, PW ;
Spencer, S ;
Anderson, JA ;
Maslen, TK .
BMJ-BRITISH MEDICAL JOURNAL, 2000, 320 (7245) :1297-1303
[5]
IRREVERSIBLE BRONCHIAL GOBLET CELL METAPLASIA IN HAMSTERS WITH ELASTASE-INDUCED PANACINAR EMPHYSEMA [J].
CHRISTENSEN, TG ;
KORTHY, AL ;
SNIDER, GL ;
HAYES, JA .
JOURNAL OF CLINICAL INVESTIGATION, 1977, 59 (03) :397-404
[6]
Superoxide dismutase expression attenuates cigarette smoke- or elastase-generated emphysema in mice [J].
Foronjy, RF ;
Mirochnitchenko, O ;
Propokenko, O ;
Lemaitre, V ;
Jia, YX ;
Inouye, M ;
Okada, Y ;
D'Armiento, JM .
AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, 2006, 173 (06) :623-631
[7]
Increased persistence of lung gene expression using plasmids containing the ubiquitin C or elongation factor 1α promoter [J].
Gill, DR ;
Smyth, SE ;
Goddard, CA ;
Pringle, IA ;
Higgins, CF ;
Colledge, WH ;
Hyde, SC .
GENE THERAPY, 2001, 8 (20) :1539-1546
[8]
HOLMGREN A, 1995, METHOD ENZYMOL, V252, P199
[9]
Redox-active protein thioredoxin prevents proinflammatory cytokine- or bleomycin-induced lung injury [J].
Hoshino, T ;
Nakamura, H ;
Okamoto, M ;
Kato, S ;
Araya, S ;
Nomiyama, K ;
Oizumi, K ;
Young, HA ;
Aizawa, H ;
Yodoi, J .
AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, 2003, 168 (09) :1075-1083
[10]
Cutting edge: IL-18-transgenic mice: In vivo evidence of a broad role for IL-18 in modulating immune function [J].
Hoshino, T ;
Kawase, Y ;
Okamoto, M ;
Yokota, K ;
Yoshino, K ;
Yamamura, K ;
Miyazaki, J ;
Young, HA ;
Oizumi, K .
JOURNAL OF IMMUNOLOGY, 2001, 166 (12) :7014-7018