Activated Syndecan-1 Shedding Contributes to Mice Colitis Induced by Dextran Sulfate Sodium
Activated Syndecan-1 Shedding Contributes to Mice Colitis Induced by Dextran Sulfate Sodium
复制标题
活化的 Syndecan-1 脱落导致葡聚糖硫酸钠诱导的小鼠结肠炎
DOI：
10.1007/s10620-010-1398-8
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发表时间：
2011-04
影响因子：
3.1
通讯作者：
Wang, Xianfei
中科院分区：
文献类型：
--
作者：
Wang, Xia;Chen, Ye;Song, Yugang;Zhang, Shaoheng;Xie, Xiaoyun;Wang, Xianfei
BackgroundSyndecan-1(Sdc1) plays important roles in many steps of inflammatory responses. In ulcerative colitis patients, decreased Sdc1 expression was observed and Sdc1 analogue heparin could improve the disease course. A better understanding of how Sdc1 functions in colitis will benefit the disease intervention.AimsTo evaluate the role of Sdc1 in dextran sulfate sodium (DSS)-induced colitis.MethodsBALB/c mice were grouped randomly into control, DSS, and heparin+DSS. The DSS group was given 4% DSS orally and heparin+DSS group was given 4% DSS with heparin (enoxaparin) subcutaneously, while the control was given distilled water orally. All mice were killed at day 7. Disease activities, histopathological changes, membrane-bound and free Sdc1 level and mRNA expression of Sdc1, IL-1, and IL-10 in colon mucosa were detected.ResultsSignificant colitis was observed in the DSS group, but disease activity index and histological score showed significant lower in the heparin+DSS group than those in the DSS group. Compared to the control group, decreased Sdc1 protein expression was detected in colon mucosa of DSS-induced colitis while Sdc1 ectodomain level in serum was much higher. Inhibited Sdc1 ectodomain shedding was detected in the heparin+DSS group compared to the DSS group. RT-PCR demonstrated that both IL-1 and IL-10 expression were up-regulated in DSS-induced colitis while heparin lessened the up-regulation extent.ConclusionsSdc1 shedding is activated in DSS-induced colitis and heparin, which mimics Sdc1 functions, relieves colitis severity by inhibiting Sdc1 shedding and down-regulating cytokines expression.
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影响因子：
3.2
作者：
Sashio, H;Tamura, K;Furuyama, J
通讯作者：
Furuyama, J
影响因子：
5.3
作者：
T. Murphy;M. Cleveland;P. Kulesza;J. Magram;K. Murphy
通讯作者：
T. Murphy;M. Cleveland;P. Kulesza;J. Magram;K. Murphy
影响因子：
7.6
作者：
Törkvist;Thorlacius;Sjöqvist;Bohman;Lapidus;Flood;Ågren;Raud;Löfberg
通讯作者：
Törkvist;Thorlacius;Sjöqvist;Bohman;Lapidus;Flood;Ågren;Raud;Löfberg
影响因子：
29.4
作者：
K. Youngman;P. Simon;G. West;F. Cominelli;D. Rachmilewitz;J. Klein;C. Fiocchi
通讯作者：
K. Youngman;P. Simon;G. West;F. Cominelli;D. Rachmilewitz;J. Klein;C. Fiocchi
影响因子：
7.6
作者：
P. Zezos;G. Papaioannou;N. Nikolaidis;K. Patsiaoura;A. Papageorgiou;T. Vassiliadis;O. Giouleme;N. Evgenidis
通讯作者：
P. Zezos;G. Papaioannou;N. Nikolaidis;K. Patsiaoura;A. Papageorgiou;T. Vassiliadis;O. Giouleme;N. Evgenidis