ArticleGastroenterology research2010
Increased Expression of Matrix Metalloproteinase-1 and 3 in Remission Patients of Steroid-Dependent Ulcerative Colitis.
Article in Gastroenterology research, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed, 6 citations in OpenAlex.
- Revisiting an Expression Dataset of Discordant Inflammatory Bowel Disease Twin Pairs Using a Mutation Burden Test RevealsFrontiers in genetics · 2021Article
- Integrated Analysis of Multiple Microarray Studies to Identify Novel Gene Signatures in Ulcerative Colitis.Frontiers in genetics · 2021Article
- Serum pharmacodynamic biomarkers for chronic corticosteroid treatment of children.Scientific reports · 2016Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundThis study was to investigate the pathological significance of protein expression of matrix metalloproteinase-1 (MMP1) and matrix metalloproteinase-3 (MMP3) in colon tissues of remission patients of steroid-dependent uncreative colitis (SDUC).
methodsTo test the possible involvement of MMP-1 and MMP-3 in SDUC, Western- blot and immunohistochemistry were applied to examine the protein expression of MMP-1 and MMP-3 in the colonic healing region from 10 remission patients with SDUC as well as from 10 remission patients with non-SDUC. Ten specimens from normal colon tissues were used as controls.
resultsCompared with the control group, the protein expression of MMP-1 and MMP-3 from non-SDUC remission patients slightly increased (p > 0.05), in contrast, those from SDUC patients significantly increased (p < 0.01).
conclusionsOver-expression of MMP-1 and MMP-3 play a critical role in the pathogenesis of SDUC.
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Registered trials
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