Overexpression of prothymosin α induces inflammatory bowel disease through regulation of matrix metalloproteinases
碩士 === 國立成功大學 === 生物化學暨分子生物學研究所 === 100 === Inflammatory bowel disease (IBD) is a group of inflammatory condition of the colon and small intestine. The major types of IBD are Crohn's disease and ulcerative colitis. It was suggested that chronic inflammation increases the risk for colon cancer....
Main Authors: | , |
---|---|
Other Authors: | |
Format: | Others |
Language: | zh-TW |
Published: |
2012
|
Online Access: | http://ndltd.ncl.edu.tw/handle/32655687309183999424 |
id |
ndltd-TW-100NCKU5104116 |
---|---|
record_format |
oai_dc |
spelling |
ndltd-TW-100NCKU51041162015-10-13T21:38:03Z http://ndltd.ncl.edu.tw/handle/32655687309183999424 Overexpression of prothymosin α induces inflammatory bowel disease through regulation of matrix metalloproteinases 過量表現前胸腺素藉由調控基質金屬蛋白酵素誘發發炎性腸道疾病 Shi-ChiHuang 黃士齊 碩士 國立成功大學 生物化學暨分子生物學研究所 100 Inflammatory bowel disease (IBD) is a group of inflammatory condition of the colon and small intestine. The major types of IBD are Crohn's disease and ulcerative colitis. It was suggested that chronic inflammation increases the risk for colon cancer. Prothymosin α (ProT) is an acid-rich non-histone nuclear protein, which is known to play an important role in proliferation, transcription, chromatin remodeling, and apoptosis. Matrix metalloproteinases (MMPs), which are zinc-dependent endopeptidases, play a major role in cell behaviors, such as cell proliferation, migration, and apoptosis. However, the regulation of MMP expression in IBD is not clear. The aim of this study is to explore the relationship between MMPs and ProT in IBD. Analysis of microarray data revealed that ProT, MMP-7, and MMP-12 were overexpressed in IBD patients. Furthermore, there were significant positive correlations between the expression levels of ProT and MMP-7 as well as ProT and MMP-12. We observed that MMPs were overexpressed in ProT homozygous transgenic mice. Using bioluminescence reporter system and immunohistochemical analysis, we found that the expression of MMP-7, MMP-12, and ProT were upregulated in the mouse IBD model induced with dextran sulfate sodium (DSS). Moreover, mice overexpressing ProT and MMP exhibited more serious IBD than the control mice. MMP-7 and MMP-12 knockout mice were resistant to DSS-induced IBD, suggesting the role of ProT, MMP-7, and MMP-12 in the development of IBD. A positive correlation between MMP and ProT expression was observed in vitro. In conclusion, our results indicate that the excess level of ProT may play an important role in the regulation of MMP-7 and MMP-12 expression in inflammatory conditions during the IBD process. Chao-Liang Wu 吳昭良 2012 學位論文 ; thesis 50 zh-TW |
collection |
NDLTD |
language |
zh-TW |
format |
Others
|
sources |
NDLTD |
description |
碩士 === 國立成功大學 === 生物化學暨分子生物學研究所 === 100 === Inflammatory bowel disease (IBD) is a group of inflammatory condition of the colon and small intestine. The major types of IBD are Crohn's disease and ulcerative colitis. It was suggested that chronic inflammation increases the risk for colon cancer. Prothymosin α (ProT) is an acid-rich non-histone nuclear protein, which is known to play an important role in proliferation, transcription, chromatin remodeling, and apoptosis. Matrix metalloproteinases (MMPs), which are zinc-dependent endopeptidases, play a major role in cell behaviors, such as cell proliferation, migration, and apoptosis. However, the regulation of MMP expression in IBD is not clear. The aim of this study is to explore the relationship between MMPs and ProT in IBD. Analysis of microarray data revealed that ProT, MMP-7, and MMP-12 were overexpressed in IBD patients. Furthermore, there were significant positive correlations between the expression levels of ProT and MMP-7 as well as ProT and MMP-12. We observed that MMPs were overexpressed in ProT homozygous transgenic mice. Using bioluminescence reporter system and immunohistochemical analysis, we found that the expression of MMP-7, MMP-12, and ProT were upregulated in the mouse IBD model induced with dextran sulfate sodium (DSS). Moreover, mice overexpressing ProT and MMP exhibited more serious IBD than the control mice. MMP-7 and MMP-12 knockout mice were resistant to DSS-induced IBD, suggesting the role of ProT, MMP-7, and MMP-12 in the development of IBD. A positive correlation between MMP and ProT expression was observed in vitro. In conclusion, our results indicate that the excess level of ProT may play an important role in the regulation of MMP-7 and MMP-12 expression in inflammatory conditions during the IBD process.
|
author2 |
Chao-Liang Wu |
author_facet |
Chao-Liang Wu Shi-ChiHuang 黃士齊 |
author |
Shi-ChiHuang 黃士齊 |
spellingShingle |
Shi-ChiHuang 黃士齊 Overexpression of prothymosin α induces inflammatory bowel disease through regulation of matrix metalloproteinases |
author_sort |
Shi-ChiHuang |
title |
Overexpression of prothymosin α induces inflammatory bowel disease through regulation of matrix metalloproteinases |
title_short |
Overexpression of prothymosin α induces inflammatory bowel disease through regulation of matrix metalloproteinases |
title_full |
Overexpression of prothymosin α induces inflammatory bowel disease through regulation of matrix metalloproteinases |
title_fullStr |
Overexpression of prothymosin α induces inflammatory bowel disease through regulation of matrix metalloproteinases |
title_full_unstemmed |
Overexpression of prothymosin α induces inflammatory bowel disease through regulation of matrix metalloproteinases |
title_sort |
overexpression of prothymosin α induces inflammatory bowel disease through regulation of matrix metalloproteinases |
publishDate |
2012 |
url |
http://ndltd.ncl.edu.tw/handle/32655687309183999424 |
work_keys_str_mv |
AT shichihuang overexpressionofprothymosinainducesinflammatoryboweldiseasethroughregulationofmatrixmetalloproteinases AT huángshìqí overexpressionofprothymosinainducesinflammatoryboweldiseasethroughregulationofmatrixmetalloproteinases AT shichihuang guòliàngbiǎoxiànqiánxiōngxiànsùjíyóudiàokòngjīzhìjīnshǔdànbáijiàosùyòufāfāyánxìngchángdàojíbìng AT huángshìqí guòliàngbiǎoxiànqiánxiōngxiànsùjíyóudiàokòngjīzhìjīnshǔdànbáijiàosùyòufāfāyánxìngchángdàojíbìng |
_version_ |
1718067394265481216 |