Inflammatory bowel disease is associated with changes of enterocytic junctions

被引:311
作者
Gassler, N
Rohr, C
Schneider, A
Kartenbeck, J
Bach, A
Overmüller, N
Otto, HF
Autschbach, F
机构
[1] Heidelberg Univ, Inst Pathol, D-69120 Heidelberg, Germany
[2] BASF LYNX Biosci AG, D-69120 Heidelberg, Germany
[3] Heidelberg Univ, Klinikum Mannheim, ZMF, D-68167 Mannheim, Germany
[4] Goethe Univ Frankfurt, Nephrol Abt, Med Klin 4, D-60590 Frankfurt, Germany
[5] Deutsch Krebsforschungszentrum, D-69120 Heidelberg, Germany
来源
AMERICAN JOURNAL OF PHYSIOLOGY-GASTROINTESTINAL AND LIVER PHYSIOLOGY | 2001年 / 281卷 / 01期
关键词
junctional proteins; Crohn's disease; ulcerative colitis;
D O I
10.1152/ajpgi.2001.281.1.G216
中图分类号
R57 [消化系及腹部疾病];
学科分类号
摘要
Changes of the intestinal mucosal barrier are considered to play a role in the pathogenesis of inflammatory bowel disease (IBD). Our experiments were designed to identify dysregulation of epithelial junctional molecules in the IBD intestinum and to address whether altered expression of these molecules is a primary event in IBD or a phenomenon secondary to the inflammatory process. Noninflamed and inactively and actively inflamed mucosal tissues from patients with ulcerative colitis or Crohn's disease as well as tissues from control subjects were analyzed for the expression of junctional molecules by different methods. Marked downregulation of junctional proteins and their respective mRNAs was observed in actively inflamed IBD tissues. In IBD tissues with inactive inflammation, only a few junctional molecules such as E-cadherin and alpha -catenin were affected, whereas expression of desmosomal or tight junction-associated proteins appeared almost unchanged. In noninflamed IBD tissues, junctional protein expression was not different from that seen in normal control subjects. In IBD, downregulation of junctional molecule expression is apparently associated with the inflammatory process and does not likely represent a primary phenomenon.
引用
收藏
页码:G216 / G228
页数:13
相关论文
共 55 条
  • [1] Interspecies diversity of the occludin sequence: cDNA cloning of human, mouse, dog, and rat-kangaroo homologues
    AndoAkatsuka, Y
    Saitou, M
    Hirase, T
    Kishi, M
    Sakakibara, A
    Itoh, M
    Yonemura, S
    Furuse, M
    Tsukita, S
    [J]. JOURNAL OF CELL BIOLOGY, 1996, 133 (01) : 43 - 47
  • [2] Rapid transepithelial antigen transport in rat jejunum: Impact of sensitization and the hypersensitivity reaction
    Berin, MC
    Kiliaan, AJ
    Yang, PC
    Groot, JA
    Taminiau, JAJM
    Perdue, MH
    [J]. GASTROENTEROLOGY, 1997, 113 (03) : 856 - 864
  • [3] Blumberg RS, 1999, FALK SYMP, V105, P155
  • [4] MOLECULAR-CLONING AND CHARACTERIZATION OF THE HUMAN E-CADHERIN CDNA
    BUSSEMAKERS, MJG
    VANBOKHOVEN, A
    MEES, SGM
    KEMLER, R
    SCHALKEN, JA
    [J]. MOLECULAR BIOLOGY REPORTS, 1993, 17 (02) : 123 - 128
  • [5] SEX STEROIDS UP-REGULATE E-CADHERIN EXPRESSION IN HORMONE-RESPONSIVE LNCAP HUMAN PROSTATE-CANCER CELLS
    CARRUBA, G
    MICELI, D
    DAMICO, D
    FARRUGGIO, R
    COMITO, L
    MONTESANTI, A
    POLITO, L
    CASTAGNETTA, LAM
    [J]. BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 1995, 212 (02) : 624 - 631
  • [6] PURIFICATION, IMMUNOASSAY, AND TISSUE DISTRIBUTION OF RAT C1-TETRAHYDROFOLATE SYNTHASE
    CHEEK, WD
    APPLING, DR
    [J]. ARCHIVES OF BIOCHEMISTRY AND BIOPHYSICS, 1989, 270 (02) : 504 - 512
  • [7] CHOMCZYNSKI P, 1993, BIOTECHNIQUES, V15, P532
  • [8] Dignass AU, 1999, FALK SYMP, V105, P188
  • [9] E-CADHERIN EXPRESSION IN INTESTINAL EPITHELIUM
    DOGAN, A
    WANG, ZD
    SPENCER, J
    [J]. JOURNAL OF CLINICAL PATHOLOGY, 1995, 48 (02) : 143 - 146
  • [10] Fries W, 1999, LAB INVEST, V79, P49