Reference maps of mouse serum acute-phase proteins: Changes with LPS-induced inflammation and apolipoprotein A-I and A-II transgenes

被引:44
作者
Wait, R
Chiesa, G
Parolini, C
Miller, I
Begum, S
Brambilla, D
Galluccio, L
Ballerio, R
Eberini, I
Gianazza, E
机构
[1] Univ Milan, Dipartimento Sci Farmacol, I-20133 Milan, Italy
[2] Univ London Imperial Coll Sci & Technol, Kennedy Inst Rheumatol Div, Fac Med, London, England
[3] Univ Milan, Grp Studio Proteom & Struttura Prot, Milan, Italy
[4] Univ Milan, Ctr Eccellenza Malattie Sistema Nervoso Cent & Pe, Milan, Italy
[5] Vet Med Univ Wien, Inst Med Chem, Dept Naturwissensch, Vienna, Austria
[6] IRCCS, Ctr Cardiol Monzino, Milan, Italy
关键词
2-DE; Mus musculus; protease inhibitors; proteome; serpins;
D O I
10.1002/pmic.200401292
中图分类号
Q5 [生物化学];
学科分类号
071010 ; 081704 ;
摘要
We present reference maps of the mouse serum proteome (run under reducing and non-reducing conditions), from control animals, from mice injected with lipopolysaccharide (LPS) to induce systemic inflammation, and from mice transgenic for human apolipoproteins A-I and A-II. Seventy-seven spots/spot chains from the reducing gels were identified by HPLC MS/MS, representing 28 distinct proteins, including a species-specific protease inhibitor, contrapsin, and high levels of carboxylesterase. The concentrations of acute-phase reactants were monitored for 96 h after LPS challenge. The greatest changes (four-fold 48 h after LPS administration) were observed for haptoglobin and hemopexin. Orosomucoid/alpha(1)-acid glycoprotein and apolipoprotein A-I increased steadily, to 50-60% above baseline at 96 h from stimulation. In mice transgenic for human apolipoprotein A-I the levels of expression of orosomucoid/alpha(1)-acid glycoprotein, alpha(1)-macroglobulin, esterase, kininogen and contrapsin were altered compared to knockout mice lacking apolipoprotein A-I. In contrast, except for the presence of apolipoprotein A-II, no statistically significant difference was observed in mice transgenic for human apolipoprotein A-II.
引用
收藏
页码:4245 / 4253
页数:9
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