Homocysteine Promotes Intestinal Fibrosis in Rats with Trinitrobenzene Sulfonic Acid-Induced Colitis

Ding, Hao; Gan, Huizhong; Fan, Wei; Cao, Lei; Xu, Jianming; Qiao, Mu

doi:10.1007/s10620-014-3379-9

Cited by 14 publications

(8 citation statements)

References 30 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The effects of homocysteine on the development of intestinal fibrosis were investigated in TNBS-induced rat model (Ding et al, 2015). Administration of homocysteine to rats with TNBS-induced colitis was found to aggravate the severity of intestinal inflammation with higher levels of TNF-α, IL-1β and IL-6.…”

Section: Involvement Of Mmps and Timps In Animal Models Of Intestinalmentioning

confidence: 99%

The molecular biology of matrix metalloproteinases and tissue inhibitors of metalloproteinases in inflammatory bowel diseases

Bruyn¹,

Vandooren

Ugarte-Berzal

et al. 2016

Critical Reviews in Biochemistry and Molecular Biology

View full text Add to dashboard Cite

Matrix metalloproteinases (MMPs) and tissue inhibitors of metalloproteinases (TIMPs) are thought to be predominant proteases and protease inhibitors involved in the pathogenesis of inflammatory bowel diseases (IBD) through their ability to remodel the extracellular matrix (ECM) in response to inflammatory stimuli and by their immunomodulating effects. An imbalance between MMPs and TIMPs has been linked with acute and chronic inflammation and aberrant tissue remodeling, as seen in IBD. Moreover, recurrent phases of tissue destruction and subsequent tissue repair can cause serious complications in IBD patients such as fistulas and fibrosis. The aims of this review are (i) to summarize current literature on genetic association, mRNA, and protein expression studies with regard to MMPs and TIMPs in IBD patients and various animal models, including those with transgenic and knockout mice; (ii) to compare biochemical and molecular biological data in humans with those obtained in animal model studies and (iii) to critically evaluate and translate how this knowledge may be used in practical terms to understand better the pathophysiology and mechanisms operating in IBD and to apply this for improvement of clinical outcomes at diagnostic, prognostic and therapeutic levels.

show abstract

Section: Involvement Of Mmps and Timps In Animal Models Of Intestinalmentioning

confidence: 99%

The molecular biology of matrix metalloproteinases and tissue inhibitors of metalloproteinases in inflammatory bowel diseases

Bruyn¹,

Vandooren

Ugarte-Berzal

et al. 2016

Critical Reviews in Biochemistry and Molecular Biology

View full text Add to dashboard Cite

show abstract

“…The results suggested that homocysteine aggravated intestinal fibrosis in rats with TNBS/ethanol-induced colitis. The mechanisms were probably due to its effects on promoting the expression of profibrogenic cytokines and influencing the MMP/TIMP balance [48]. The possibility of the anti-fibrotic activity of HGF in the liver was indicated [49].…”

Section: Discussionmentioning

confidence: 99%

Hepatocyte Growth Factor Facilitates Esophageal Mucosal Repair and Inhibits the Submucosal Fibrosis in a Rat Model of Esophageal Ulcer

et al. 2018

View full text Add to dashboard Cite

Background/Aims: Esophageal mucosal damage often causes scar tissue, leading to refractory stricture. The aim of this study was to clarify the effect of hepatocyte growth factor (HGF) on esophageal mucosal repair and fibrosis leading to stricture in a rat model of esophageal ulcer. Methods: Esophageal ulcers were induced in rats by topical exposure of the lower esophageal serosa to acetic acid, followed by intraperitoneal administration of HGF (200 µg/day) using an osmotic pump for 7 days. The effect of HGF on esophageal mucosal injury was investigated macroscopically and microscopically. The effect of HGF on epithelial cell proliferation and the expression of genes closely associated with the development of fibrosis were also examined. Results: The administration of HGF for 7 days led to a significant reduction in the ulcerative area and enhanced the proliferation of esophageal epithelial cells. HGF treatment significantly decreased the fibrosis, and subsequently attenuated not only the foreshortening but also the narrowing of the esophagus. The expression levels of tissue inhibitor of metalloproteinase (TIMP)-1, -2, and matrix metalloproteinase (MMP)-2, -9 were significantly decreased among rats treated with HGF. Conclusion: HGF facilitates the repair of esophageal mucosal injury and may also ameliorate the esophageal fibrosis, possibly through enhanced re-epithelization.

show abstract

“…On the other hand, the increased expression of matrix metalloproteinase (MMP) and the decreased expression of tissue inhibitor of metalloproteinase (TIMP) and tight junction proteins (zonula occluden-1) indicate vascular remodelling. Hcy promots the expression of profibrogenic cytokines and influences the MMP/TIMP balance 40 . The MMP is known to regulate the activities of collagenase and gelatinase 41 .…”

Section: Discussionmentioning

confidence: 99%

Homocysteine in retinal artery occlusive disease: A meta-analysis of cohort studies

Huang

Yang

Duan

et al. 2017

Sci Rep

View full text Add to dashboard Cite

Few studies have reported the relationship between retinal artery occlusion (RAO) and plasma homocysteine (Hcy) levels. Our goal was to evaluate the association between the plasma Hcy level and the risk of RAO disease. Several databases were searched for all published studies that involved Hcy and RAO. Six studies evaluated hyperhomocysteinemia (hHcy) in retinal artery occlusion patients and controls; the incidence of hHcy in patients with RAO was higher than the control and the pooled odds ratio (OR) was 6.64 (95% confidence interval (CI): 3.42, 12.89). Subgroup analyses showed that the ORs were 4.77 (95% CI: 2.69, 8.46) in Western countries, 22.19 (95% CI: 2.46, 200.37) in Asian countries, 9.70 (95% CI: 4.43, 21.20) in the age matched group, 11.41 (95% CI: 3.32, 39.18) in the sex matched group, 9.70 (95% CI: 4.37, 21.53) in the healthy control group, and 6.82 (95% CI: 4.19, 11.10) in the sample size >30. The mean plasma Hcy level from 5 case-control studies was higher than controls, and the weighted mean difference (WMD) was 6.54 (95% CI: 2.79, 10.29). Retinal artery occlusion is associated with elevated plasma Hcy levels. Our study results suggest that hHcy is probably an independent risk factor for RAO.

show abstract

Homocysteine Promotes Intestinal Fibrosis in Rats with Trinitrobenzene Sulfonic Acid-Induced Colitis

Abstract: Hcy promotes intestinal fibrosis in rats with TNBS/ethanol-induced colitis, the underlying mechanisms of which may be attributed to its effects of increasing inflammatory damage, promoting the expression of profibrogenic cytokines and influencing MMPs/TIMPs balance.

Cited by 14 publications

References 30 publications

The molecular biology of matrix metalloproteinases and tissue inhibitors of metalloproteinases in inflammatory bowel diseases

The molecular biology of matrix metalloproteinases and tissue inhibitors of metalloproteinases in inflammatory bowel diseases

Hepatocyte Growth Factor Facilitates Esophageal Mucosal Repair and Inhibits the Submucosal Fibrosis in a Rat Model of Esophageal Ulcer

Homocysteine in retinal artery occlusive disease: A meta-analysis of cohort studies

Contact Info

Product

Resources

About