Measurement of matrix-metalloproteinase-mRNA-expression in single biopsies of patients with chronic inflammatory bowel diseases by competitive PCR

Lampe, B; Barthel, Brandon; Riecken, E. O.; Rosewicz, Stefan

doi:10.1016/s0016-5085(98)84518-6

Cited by 5 publications

(12 citation statements)

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“…34) One study has reported a more than 15-fold greater expression of MMP1 and MMP3 mRNA in inflamed colon than in normal colon samples from patients with ulcerative colitis and Crohn's disease. 35) A DPPIV deficiency might affect the differentiation and functions of macrophages and suppress immune responses, resulting in a retardation of the experimental colitis. Immune suppression might suggest an additional future use of DPPIV inhibitors in autoimmune diseases or transplantation.…”

Section: Discussionmentioning

confidence: 99%

Contribution of Dipeptidyl Peptidase IV to the Severity of Dextran Sulfate Sodium-Induced Colitis in the Early Phase

Iwaya

Fujii

Hagio

et al. 2013

Bioscience, Biotechnology, and Biochemistry

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Section: Discussionmentioning

confidence: 99%

Contribution of Dipeptidyl Peptidase IV to the Severity of Dextran Sulfate Sodium-Induced Colitis in the Early Phase

Iwaya

Fujii

Hagio

et al. 2013

Bioscience, Biotechnology, and Biochemistry

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“…Moreover, elevated MMP-3 mRNA levels in CD patients with active disease returned to normal following treatment with enteral nutrition (Heuschkel et al, 2000). In inflamed colon samples from patients with UC and CD, MMP-1 and -3 mRNA expression was described to be more than 15-fold increased compared with normal colon samples and the levels correlated well with the histological degree of acute inflammation (von Lampe et al, 2000). The expression of MMP-2 and -14 mRNAs was found to be marginally increased in inflamed, but 9-12-fold increased in ulcerated colonic mucosa of IBD patients.…”

Section: Targeted Mrna Expression Studiesmentioning

confidence: 91%

“…A wide range of cell types have been shown to express MMPs, including epithelial cells, mesenchymal cells and leukocytes (Kirkegaard et al, 2004;Kruidenier et al, 2006;Matsuno et al, 2003;McKaig et al, 2003;O'Sullivan et al, 2015;Pedersen et al, 2009;Saarialho-Kere et al, 1996;Vaalamo et al, 1998;von Lampe et al, 2000). Moreover, Ravi et al have elaborately studied the expression of MMPs in IBD and described the cellular source and function of MMPs in normal conditions and in IBD (Ravi et al, 2007).…”

Section: Mmp Protein Expression Studiesmentioning

confidence: 99%

The molecular biology of matrix metalloproteinases and tissue inhibitors of metalloproteinases in inflammatory bowel diseases

Bruyn¹,

Vandooren

Ugarte-Berzal

et al. 2016

Critical Reviews in Biochemistry and Molecular Biology

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Matrix metalloproteinases (MMPs) and tissue inhibitors of metalloproteinases (TIMPs) are thought to be predominant proteases and protease inhibitors involved in the pathogenesis of inflammatory bowel diseases (IBD) through their ability to remodel the extracellular matrix (ECM) in response to inflammatory stimuli and by their immunomodulating effects. An imbalance between MMPs and TIMPs has been linked with acute and chronic inflammation and aberrant tissue remodeling, as seen in IBD. Moreover, recurrent phases of tissue destruction and subsequent tissue repair can cause serious complications in IBD patients such as fistulas and fibrosis. The aims of this review are (i) to summarize current literature on genetic association, mRNA, and protein expression studies with regard to MMPs and TIMPs in IBD patients and various animal models, including those with transgenic and knockout mice; (ii) to compare biochemical and molecular biological data in humans with those obtained in animal model studies and (iii) to critically evaluate and translate how this knowledge may be used in practical terms to understand better the pathophysiology and mechanisms operating in IBD and to apply this for improvement of clinical outcomes at diagnostic, prognostic and therapeutic levels.

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“…Their activity is tightly controlled by the tissue-specific inhibitors of metalloproteases (TIMPs) which are produced by the same cells that make MMPs. Therefore, changes in the balance between MMPs and TIMPs production/activity can contribute either to the mucosal degradation or remodeling occurring in IBD [29][30][31][32]. Importantly, fibroblasts produce MMPs and/or collagen following in vitro exposure to cytokines made by T cells and macrophages, thus indicating that this is a typical response to inflammatory stimuli [33].…”

Section: Il-21 Enhances Matrix Metalloproteases Secretion By Gut Fibrmentioning

confidence: 99%

Interleukin-21 (IL-21) Controls Inflammatory Pathways in the Gut

Fina¹,

Caruso²,

Pallone³

et al. 2007

EMIDDT

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In both Crohn's disease (CD) and ulcerative colitis (UC), the major forms of inflammatory bowel diseases (IBD) in humans, the pathologic process consists of an aberrant local immune response to components of the bacterial microflora, due to abnormally strong effector cell activity that is poorly controlled by counter-regulatory mechanisms. There is also evidence that mucosal immune cells actively interact with non-immune cells to promote tissue damage, and that cytokines are essential mediators of this cross-talk. Interleukin-21 (IL-21), the latest member of the common gamma-chain-dependent cytokine family, is a product of activated CD4+ T cells and natural killer T cells. IL-21 is produced in excess in CD tissue, where it helps sustain the ongoing Th1 inflammation. High IL-21 production occurs also in the inflamed colon of most patients with UC, a disease that is not associated with a marked Th1 cell response. This suggests that, in the gut, IL-21 can modulate additional inflammatory pathways other than enhancing Th1 cell immunity. Indeed, IL-21 stimulates the secretion of extracellular matrix degrading enzymes by fibroblasts, and of the T cell chemoattractant, MIP-3 alpha, by epithelial cells. These data collectively indicate that IL-21 is a mediator of the chronic inflammatory response in CD and UC, and suggest that IL-21 may be an emerging therapeutic target in IBD.

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Measurement of matrix-metalloproteinase-mRNA-expression in single biopsies of patients with chronic inflammatory bowel diseases by competitive PCR

Cited by 5 publications

References 0 publications

Contribution of Dipeptidyl Peptidase IV to the Severity of Dextran Sulfate Sodium-Induced Colitis in the Early Phase

Contribution of Dipeptidyl Peptidase IV to the Severity of Dextran Sulfate Sodium-Induced Colitis in the Early Phase

The molecular biology of matrix metalloproteinases and tissue inhibitors of metalloproteinases in inflammatory bowel diseases

Interleukin-21 (IL-21) Controls Inflammatory Pathways in the Gut

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