scholarly journals Dextran sulfate sodium-induced colitis mice up-regulated extracellular matrix tenascin-C

2017 ◽  
Vol 2 (4) ◽  
pp. 582-586
Author(s):  
Md Shafiqul Islam ◽  
Masatoshi Hori ◽  
Hiroshi Ozaki
Keyword(s):  
Extracellular Matrix ◽  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
Tissue Injury ◽  
Goblet Cells ◽  
Mucosal Damage ◽  
Postnatal Life ◽  
Tenascin C ◽  
Moderate Staining ◽  
High Level

Tenascin-C, an extracellular matrix glycoprotein, expresses high level during embryogenesis and almost absent during the normal postnatal life. However, it is re-appeared in a diverse condition such as tissue injury and in the stroma of various carcinomas. In this study, we investigated the appearance of tenascin-C in dextran sulfate sodium (DSS)-induced colitis in mice. DSS induced colitis mice demonstrated severe mucosal damage, with distortion and loss of crypts, depletion of goblet cells and infiltration of macrophages particularly F4/80 positive macrophages, granulocytes and lymphocytes in the colon tissues. These DSS inflamed colon expressed a high and dense level of tenascin-C in the severe damaged areas, whereas, moderate staining was observed in the moderate inflamed areas. DSS-induced colitis mice significantly increased macrophages infiltration in the colon tissues. These results suggested that tenascin-C extracellular matrix re-appeared in the colon tissues during inflammation.Asian J. Med. Biol. Res. December 2016, 2(4): 582-586

Deficiency of extracellular matrix integrin α1β1 protects mice against dextran sulfate sodium induced colitis

2001 ◽  
Vol 120 (5) ◽  
pp. A522
Author(s):  
Christian F. Krieglstein ◽  
Stephen F. Laroux ◽  
Wun L. Chang ◽  
Matthew B. Grisham ◽  
Guido M. Schuermann ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Dextran Sulfate ◽  
Dextran Sulfate Sodium

scholarly journals Mice Deficient in Cyp4a14 Have An Increased Number of Goblet Cells and Attenuated Dextran Sulfate Sodium-Induced Colitis

2018 ◽  
Vol 50 (6) ◽  
pp. 2272-2282 ◽  
Author(s):  
Qingxia Xuan ◽  
Yunfeng Zhou ◽  
Binbin Tan ◽  
Zhongyue Xiao ◽  
Shizhen Dong ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
Quantitative Polymerase Chain Reaction ◽  
Periodic Acid ◽  
Mucosal Injury ◽  
Goblet Cells ◽  
Mrna Levels ◽  
Periodic Acid Schiff ◽  
Monooxygenase Activity

Background/Aims: Cyp4a14 is a member of cytochrome P450 (Cyp450) enzyme superfamily that possesses NADPH monooxygenase activity, which catalyzes omega-hydroxylation of medium-chain fatty acids and arachidonic acid. Study suggests that down-regulation of Cyp4a14 has an anti-inflammatory response in intestine. The present study was to test the function of Cyp4a14 in dextran sulfate sodium (DSS)-induced colitis. Methods: Female Cyp4a14-knockout (KO) and wild-type (WT) mice were treated with DSS for 6 days to induce colitis. The colon of mice was histologically observed by hematoxylin and eosin (H&E) and periodic acid Schiff (PAS) staining. The serum malondialdehyde (MDA), an endogenous indicator of oxidative stress, was chemically measured. Proinflammatory and NADPH oxidase genes were examined by quantitative polymerase chain reaction (qPCR). Results: Cyp4a14-KO mice had a significantly higher number of goblet cells in the colon and were more resistant to DSS-induced colitis compared with the WT mice. The DSS-treated KO mice had lower levels of MDA. Consistent with the milder inflammatory pathological changes, DSS-treated KO mice had lower levels of IL-1β, IL-6 and TNF-α mRNA in the liver and the colon. Moreover, the colon of DSS-treated Cyp4a14-KO and WT mice had higher mRNA levels of two members of NADPH oxidases, Nox2 and Nox4, suggesting that both Nox2 and Nox4 are inflammatory markers. By contrast, DSS-treated WT and KO mice had drastically decreased epithelium-localized Nox1 and dual oxidase (Duox) 2 mRNA levels, coinciding with the erosion of the mucosa induced by DSS. Conclusion: These results suggests a hypothesis that the increased goblet cell in the colon of Cyp4a14-KO mice provides protection from mucosal injury and Cyp4a14-increased oxidative stress exacerbates DSS-induced colitis. Therefore, Cyp4a14 may represent a potential target for treating colitis.

Su1896 Tenascin-C Mediates the Suppressive Effects on Inflammation by the Mesenchymal Stem Cell in Dextran Sulfate Sodium Induced Colitis

2015 ◽  
Vol 148 (4) ◽  
pp. S-547 ◽  
Author(s):  
Atsushi Hoshino ◽  
Hisashi Hashimoto ◽  
Seiji Arihiro ◽  
Hiroshi ozaki ◽  
Masatoshi Hori ◽  
...  
Keyword(s):  
Stem Cell ◽  
Mesenchymal Stem Cell ◽  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
Tenascin C

Deficiency of extracellular matrix integrin α1β1 protects mice against dextran sulfate sodium induced colitis

2001 ◽  
Vol 120 (5) ◽  
pp. A522-A522
Author(s):  
C KRIEGLSTEIN ◽  
S LAROUX ◽  
W CHANG ◽  
M GRISHAM ◽  
G SCHUERMANN ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Dextran Sulfate ◽  
Dextran Sulfate Sodium

scholarly journals Polyphenol Extract of Moringa Oleifera Leaves Alleviates Colonic Inflammation in Dextran Sulfate Sodium-Treated Mice

2020 ◽  
Vol 2020 ◽  
pp. 1-9
Author(s):  
Yunjuan Zhang ◽  
Lei Peng ◽  
Wenyun Li ◽  
Tianyi Dai ◽  
Long Nie ◽  
...  
Keyword(s):  
Moringa Oleifera ◽  
Dextran Sulfate ◽  
Dextran Sulfate Sodium ◽  
Activity Index ◽  
Disease Activity Index ◽  
Experimental Colitis ◽  
Mucosal Damage ◽  
Tnf Α ◽  
Moringa Oleifera Leaves ◽  
Moringa Oleifera Lam

Moringa oleifera Lam. is an essential herb used for the treatment of inflammation, diabetes, high blood pressure, and other diseases. In this study, phenolic extracts of M. oleifera leaves were obtained and analyzed. The results showed that the main identifiable phenols were astragalin, chlorogenic acid, isoquercitrin, kaempferitrin, luteolin, quercetin, and rutin. The effects of M. oleifera polyphenol extract (MOPE) on experimental colitis induced by 3% dextran sulfate sodium (DSS) were investigated. The results showed that oral administration of MOPE significantly alleviated the symptoms of DSS-induced colitis. MOPE significantly reduced weight loss, the disease activity index, colon shortening, and mucosal damage. In addition, MOPE attenuated the infiltration of CD3+ T cells, CD177+ neutrophils, and F4/80+ macrophages and significantly inhibited the secretion of IL-6 and TNF-α. After the MOPE administration, the expression of proteins associated with the NF-κB signaling pathway changed. Specifically, compared with that of the DSS group, the protein expression of NF-κB p65 and p-IκBα was downregulated, and the expression of IκBα was upregulated. This study revealed the anti-inflammatory effects and mechanisms of MOPE in the colon, indicating its potential use in preventing inflammation-driven diseases.

scholarly journals Coregulation of Fibronectin Signaling and Matrix Contraction by Tenascin-C and Syndecan-4

2004 ◽  
Vol 15 (12) ◽  
pp. 5670-5677 ◽  
Author(s):  
Kim S. Midwood ◽  
Leyla V. Valenick ◽  
Henry C. Hsia ◽  
Jean E. Schwarzbauer
Keyword(s):  
Extracellular Matrix ◽  
Intracellular Signaling ◽  
Tissue Repair ◽  
Matrix Protein ◽  
Tissue Injury ◽  
Fiber Formation ◽  
Extracellular Matrix Protein ◽  
Actin Stress Fiber ◽  
Tenascin C ◽  
Matrix Contraction

Syndecan-4 is a ubiquitously expressed heparan sulfate proteoglycan that modulates cell interactions with the extracellular matrix. It is transiently up-regulated during tissue repair by cells that mediate wound healing. Here, we report that syndecan-4 is essential for optimal fibroblast response to the three-dimensional fibrin-fibronectin provisional matrix that is deposited upon tissue injury. Interference with syndecan-4 function inhibits matrix contraction by preventing cell spreading, actin stress fiber formation, and activation of focal adhesion kinase and RhoA mediated-intracellular signaling pathways. Tenascin-C is an extracellular matrix protein that regulates cell response to fibronectin within the provisional matrix. Syndecan-4 is also required for tenascin-C action. Inhibition of syndecan-4 function suppresses tenascin-C activity and overexpression of syndecan-4 circumvents the effects of tenascin-C. In this way, tenascin-C and syndecan-4 work together to control fibroblast morphology and signaling and regulate events such as matrix contraction that are essential for efficient tissue repair.

Shikonin inhibits colitis-associated colorectal dysplasias in a mouse model of azoxymethane/dextran sulfate sodium colitis

Planta Medica ◽  
2012 ◽  
Vol 78 (11) ◽  
Author(s):  
JL Ríos ◽  
A Martí ◽  
I Andújar ◽  
RM Giner ◽  
MC Recio
Keyword(s):  
Mouse Model ◽  
Dextran Sulfate ◽  
Dextran Sulfate Sodium
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