Distinct gene expression of osteopontin in patients with ulcerative colitis

被引:32
作者
Masuda, H
Takahashi, Y
Asai, S
Takayama, T
机构
[1] Nihon Univ, Sch Med, Dept Surg 3, Nerima Ku, Tokyo 1790072, Japan
[2] Nihon Univ, Sch Med, Med Res Ctr, Div Genet & Genom Med, Tokyo 1790072, Japan
关键词
oligonucleotide arrays; gene expression; ulcerative colitis; inflammatory bowel disease; osteopontin; macrophage metalloelastase;
D O I
10.1016/S0022-4804(03)00046-5
中图分类号
R61 [外科手术学];
学科分类号
摘要
Background. Ulcerative colitis (UC) is a multifactorial disorder of unknown etiology. Few studies have applied genome-wide gene expression analysis in colon tissue samples of UC. We report the analysis of mucosal gene expression in UC and noninflamed control specimens. Materials and methods. This study included 7 UC patients who received a total colectomy because of severe total colitis. Normal control colon tissues were obtained at least 10 cm from the area of pathology in 3 colon cancer patients. Ten colonic tissue samples (7 UC and 3 normal control samples) were subjected to high-density oligonucleotide array analysis. To compare differences in the level of gene expression between UC and control samples, Mann-Whitney U-test was used, with significance set at P < 0.05. Results. Twenty-five genes had a 3.0similar to23.4-fold higher mRNA expression in UC samples compared with normal samples, whereas three genes had a 3.0 similar to 3.4-fold lower expression in UC samples compared with normal samples. Two genes showing more than a 10-fold increase expression in UC samples were a macrophage metalloelastase (L23808) and a osteopontin (AF052124). It has been said that macrophage metalloelastase is related to ulcer formation of the intestine, whereas osteopontin plays an important role in the pathogenesis of systemic lupus erythematosus and rheumatoid arthritis. Conclusion. Our present study supports the previous report that macrophage metalloelastase is related to ulcer formation of UC, and it also indicates the possibility that osteopontin plays an important role in the pathogenesis of UC via increased immune activity. (C) 2003 Elsevier Inc. All rights reserved.
引用
收藏
页码:85 / 90
页数:6
相关论文
共 35 条
[1]   TLR4 and MD-2 expression is regulated by immune-mediated signals in human intestinal epithelial cells [J].
Abreu, MT ;
Arnold, ET ;
Thomas, LS ;
Gonsky, R ;
Zhou, YH ;
Hu, B ;
Arditi, M .
JOURNAL OF BIOLOGICAL CHEMISTRY, 2002, 277 (23) :20431-20437
[2]   Vascular smooth muscle cells and pericytes express MMP-1, MMP-9, TIMP-1 and type I procollagen in inflammatory bowel disease [J].
Arihiro, S ;
Ohtani, H ;
Hiwatashi, N ;
Torii, A ;
Sorsa, T ;
Nagura, H .
HISTOPATHOLOGY, 2001, 39 (01) :50-59
[3]   Options available - from start to finish - for obtaining expression data by microarray [J].
Bowtell, DDL .
NATURE GENETICS, 1999, 21 (Suppl 1) :25-32
[4]   Exploring the new world of the genome with DNA microarrays [J].
Brown, PO ;
Botstein, D .
NATURE GENETICS, 1999, 21 (Suppl 1) :33-37
[5]   Increased serum levels of eotaxin in patients with inflammatory bowel disease [J].
Chen, W ;
Paulus, B ;
Shu, D ;
Wilson, I ;
Chadwick, V .
SCANDINAVIAN JOURNAL OF GASTROENTEROLOGY, 2001, 36 (05) :515-520
[6]   Making and reading microarrays [J].
Cheung, VG ;
Morley, M ;
Aguilar, F ;
Massimi, A ;
Kucherlapati, R ;
Childs, G .
NATURE GENETICS, 1999, 21 (Suppl 1) :15-19
[7]   Human phosphoglucose isomerase: expression, purification, crystallization and preliminary crystallographic analysis [J].
Cordeiro, AT ;
Godoi, PHC ;
Delboni, LF ;
Oliva, G ;
Thiemann, OH .
ACTA CRYSTALLOGRAPHICA SECTION D-STRUCTURAL BIOLOGY, 2001, 57 :592-595
[8]  
Dieckgraefe BK, 2000, PHYSIOL GENOMICS, V4, P1
[9]   High-density genome scan in Crohn disease shows confirmed linkage to chromosome 14q11-12 [J].
Duerr, RH ;
Barmada, MM ;
Zhang, LL ;
Pfützer, R ;
Weeks, DE .
AMERICAN JOURNAL OF HUMAN GENETICS, 2000, 66 (06) :1857-1862
[10]   Linkage and association between inflammatory bowel disease and a locus on chromosome 12 [J].
Duerr, RH ;
Barmada, MM ;
Zhang, LL ;
Davis, S ;
Preston, RA ;
Chensny, LJ ;
Brown, JL ;
Ehrlich, GD ;
Weeks, DE ;
Aston, CE .
AMERICAN JOURNAL OF HUMAN GENETICS, 1998, 63 (01) :95-100