scholarly journals Transcription factor paired related homeobox 1 (PRRX1) activates matrix metalloproteinases (MMP)13, which promotes the dextran sulfate sodium-induced inflammation and barrier dysfunction of NCM460 cells

Bioengineered ◽  
2021 ◽  
Vol 13 (1) ◽  
pp. 645-654
Xiujing Zhang ◽  
Lizhuan Ma ◽  
Ying Shen ◽  
Chao Zhang ◽  
Bingxu Hou ◽  
2021 ◽  
Xuemeng Si ◽  
Ning Liu ◽  
Hai Jia ◽  
Jiaqi Wang ◽  
Lina Pan ◽  

Gut relief formula administration alleviated mucosal inflammation and mucosal barrier dysfunction by inhibiting STAT3 and NF-κB activity and upregulating abundances of Lactobacillus in DSS-induced colitis.

2018 ◽  
Vol 98 (4) ◽  
pp. 462-476 ◽  
Xiangming Ding ◽  
Dongxiao Li ◽  
Mengke Li ◽  
Han Wang ◽  
Qin He ◽  

2014 ◽  
Vol 13 (4) ◽  
pp. 858-869 ◽  
Jing-jing KANG ◽  
De-ming ZHAO ◽  
Ke-dao TENG ◽  
Xi-lan JIAO ◽  
Ping-li WANG ◽  

2015 ◽  
Vol 465 (3) ◽  
pp. 503-515 ◽  
Geetha Samak ◽  
Kamaljit K. Chaudhry ◽  
Ruchika Gangwar ◽  
Damodaran Narayanan ◽  
Jonathan H. Jaggar ◽  

Delineation of the signalling mechanism involved in disruption of epiithelial tight junctions by DSS, a widely used chemical stress in inducing ulcerative colitis. This study shows that calcium/Ask1/MKK7/JNK2/cSrc signalling cascade mediates DSS-induced intestinal epithelial tight junction disruption and barrier dysfunction.

2000 ◽  
Vol 278 (5) ◽  
pp. G797-G804 ◽  
Jorge A. Marrero ◽  
Kristina A. Matkowskyj ◽  
Kenny Yung ◽  
Gail Hecht ◽  
Richard V. Benya

Galanin is widely distributed in enteric nerve terminals and acts to modulate intestinal motility by altering smooth muscle contraction. This ligand causes Cl−secretion when colonic epithelial cells express the galanin-1 receptor (Gal1-R) subtype. Because Gal1-R expression by colonic epithelia is upregulated by the transcription factor nuclear factor-κB (NF-κB), increasingly appreciated as critical in the pathophysiology of inflammatory bowel disease, we wondered whether the diarrhea associated with this condition could be due to NF-κB-mediated increases in Gal1-R expression. To test this hypothesis, we provided oral dextran sulfate sodium (DSS) to C57BL/6J mice. Although Gal1-R are not normally expressed by epithelial cells lining the mouse colon, DSS treatment resulted in increased NF-κB activation and Gal1-R expression. Whereas galanin had no effect on murine colonic tissues studied ex vivo, it progressively increased short-circuit current and colonic fluid secretion in DSS-treated mice. Concomitant parenteral administration of the NF-κB inhibitor dexamethasone attenuated the activation of this transcription factor by DSS, inhibiting the increase in Gal1-R expression. Although Gal1-R-specific antagonists do not exist, intracolonic administration of commercially available galanin antibody diminished the DSS-induced increase in colonic fluid accumulation. Overall, these data demonstrate that a significant component of the excessive fluid secretion observed in DSS-treated mice is due to increased Gal1-R expression.

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