Please use this identifier to cite or link to this item:
|標題:||Intra-abdominal adhesion formation induces anti-oxidative injury, enhances cell proliferation, and prevents complement-mediated lysis||作者:||Yu, S.L.
|關鍵字:||gene-expression;patterns;growth;differentiation;transcription;microarray;induction;relevance;discovery;cancer||Project:||Wound Repair and Regeneration||期刊/報告no：:||Wound Repair and Regeneration, Volume 16, Issue 3, Page(s) 388-398.||摘要:||
Whether the alteration of gene expression is accompanied with intra-abdominal adhesion formation is unclear. The aim of this study was to analyze the dynamic gene expression patterns in an animal model of intra-abdominal adhesion formation. The mRNA was extracted from the jejunums of sham control mice and jejunum-abrading mice at 1, 3, 7, and 14 days postsurgery. The mouse cDNA microarray was used to monitor the dynamic changes of the tested genes and up-regulated and down-regulated genes were calculated. Quantitative real-time RT-PCR, and immunohistochemistry staining were used to confirm the accuracy of microarray results at RNA and protein levels. The top 100 genes with the greatest change across all studied mice groups were identified and 93 of them were correct after sequencing verification. Of the 93 genes, 74 genes were up-regulated and 19 were down-regulated following jejunal abrasion. Gene expressions of complement-mediated lysis, anti-oxidative response, and cell proliferation were significantly induced during adhesion formation. Intra-abdominal adhesion induces several genes to eliminate overfilled complement-mediated lysis, prevent oxidative injuries, and enhance cell proliferation. These findings may provide insights into the pathogenesis of intra-abdominal adhesion formation and might also help to identify some new target genes for specific diagnostic tools and novel therapeutic strategies.
|Appears in Collections:||生物醫學研究所|
Show full item record
TAIR Related Article
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.