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角质形成细胞生长因子在炎症性肠病中高度过表达。

Keratinocyte growth factor is highly overexpressed in inflammatory bowel disease.

作者信息

Brauchle M, Madlener M, Wagner A D, Angermeyer K, Lauer U, Hofschneider P H, Gregor M, Werner S

机构信息

Max-Planck-Institut für Biochemie, Martinstried, Germany.

出版信息

Am J Pathol. 1996 Aug;149(2):521-9.

PMID:8701991
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1865327/
Abstract

Recently we demonstrated an important function of keratinocyte growth factor (KGF) in wound re-epithelialization. As KGF is mitogenic for various epithelial cells, we speculated about a role of KGF in epithelial repair processes of other organs as seen in a variety of inflammatory diseases. Here we demonstrate a strikingly increased expression of KGF in surgical specimens from patients suffering from Crohn's disease and ulcerative colitis. The levels of KGF expression strongly correlated with the degree of inflammation as assessed by histological analysis of adjacent tissue and expression analysis of the pro-inflammatory cytokine interleukin-1 beta. The highest levels of KGF mRNA and protein were found in mesenchymal cells of the lamina propria, particularly in highly inflamed areas. As the KGF receptor is expressed in intestinal epithelial cells, KGF seems to act in a paracrine manner to stimulate proliferation of these cells. These data suggest a crucial role of KGF in epithelial repair after injury caused by inflammatory processes.

摘要

最近我们证明了角质形成细胞生长因子(KGF)在伤口再上皮化过程中的重要作用。由于KGF对各种上皮细胞具有促有丝分裂作用,我们推测KGF在多种炎症性疾病中其他器官的上皮修复过程中发挥作用。在此我们证明,克罗恩病和溃疡性结肠炎患者手术标本中KGF的表达显著增加。通过对相邻组织的组织学分析和促炎细胞因子白细胞介素-1β的表达分析评估,KGF的表达水平与炎症程度密切相关。KGF mRNA和蛋白的最高水平出现在固有层的间充质细胞中,尤其是在高度炎症区域。由于KGF受体在肠道上皮细胞中表达,KGF似乎以旁分泌方式刺激这些细胞的增殖。这些数据表明KGF在炎症过程所致损伤后的上皮修复中起关键作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/83ff/1865327/8dd84c0a107c/amjpathol00032-0179-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/83ff/1865327/f004917f68f1/amjpathol00032-0175-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/83ff/1865327/a7cb2599deab/amjpathol00032-0176-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/83ff/1865327/abd7fe054d23/amjpathol00032-0177-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/83ff/1865327/080972f17483/amjpathol00032-0177-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/83ff/1865327/d9ac2b3d0640/amjpathol00032-0178-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/83ff/1865327/8dd84c0a107c/amjpathol00032-0179-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/83ff/1865327/f004917f68f1/amjpathol00032-0175-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/83ff/1865327/a7cb2599deab/amjpathol00032-0176-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/83ff/1865327/abd7fe054d23/amjpathol00032-0177-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/83ff/1865327/080972f17483/amjpathol00032-0177-b.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/83ff/1865327/d9ac2b3d0640/amjpathol00032-0178-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/83ff/1865327/8dd84c0a107c/amjpathol00032-0179-a.jpg

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Developmental localization of the splicing alternatives of fibroblast growth factor receptor-2 (FGFR2).
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