Role of anti-angiogenic factor endostatin in the pathogenesis of experimental ulcerative colitis

Tolstanova, Ganna; Deng, Xiaoming; Khomenko, Tetyana; Garg, Pallavi; Paunovic, Brankica; Chen, Longchuan; Sitaraman, Shanthi V.; Shiloach, Joseph; Szabó, Sándor; Sandor, Zsuzsanna

doi:10.1016/j.lfs.2010.10.026

Cited by 23 publications

(20 citation statements)

References 51 publications

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“…However, since the results on circulating levels of VEGF-A in UC and CD are not totally unequivocal—the majority [41–43], but not all of them [44], demonstrate elevated levels of this factor—it seems that this aspect requires further elucidation in a larger scale systematic research. This issue appears to be important especially in light of recent studies of Tolstanova et al [45] who demonstrated concomitant upregulation of MMP-9, VEGF-A, PDGF-BB, and endostatin in rodent models of UC. They suggested that the increase in endostatin plays a protective role against increased level of VEGF in UC and that MMP-9, which generates endostatin, is a key enzyme responsible for the balance between those two cytokines.…”

Section: Discussionmentioning

confidence: 99%

Matrix Metalloproteinase-9: Its Interplay with Angiogenic Factors in Inflammatory Bowel Diseases

et al. 2014

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Matrix metalloproteinase- (MMP-) 9 is one of the main metalloproteinases reported to be involved in extracellular matrix degradation and recently also in triggering of angiogenic switch in the course of inflammatory bowel diseases (IBD). The goal of our studies was to estimate in one experimental setting the levels of MMP-9 in sera of Crohn's Disease (CD) and ulcerative colitis (UC) patients and to evaluate its possible diagnostic potential in comparison with other biochemical markers and selected proinflammatory and angiogenic factors. The study group included 176 subjects (CD = 64, UC = 85, control = 27). Concentrations of serum MMP-9 were significantly higher in active than inactive forms of IBD, being higher in active UC than in active CD. Both in the case of CD and UC serum MMP-9 positively correlated with disease activity, IL-6 levels, platelet and leukocyte count, midkine, and PDGF-BB, as well as in UC with ESR and in CD with CRP, IL-1, and VEGF-A. Diagnostic accuracy of MMP-9 in distinguishing active UC from active CD was 66%, and displayed higher specificity than CRP (79.0% versus 61.6%, resp.). Evaluation of serum MMP-9 concentrations could aid in differentiation of active UC from active CD. MMP-9 correlated better with inflammatory and angiogenic parameters in CD than in UC.

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Section: Discussionmentioning

confidence: 99%

Matrix Metalloproteinase-9: Its Interplay with Angiogenic Factors in Inflammatory Bowel Diseases

et al. 2014

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“…These observations have suggested that the inflamed colonic mucosa undergoing inflammation and healing is subject to the proangiogenic and antiangiogenic signals [31]. Tolstanova et al [33] have suggested that the antiangiogenic activity of endostatin may be an intrinsic protective mechanism in ulcerative colitis. The effect of preventive VEGF inhibition on the activity and expression of intrinsic angiogenic inhibitors should be further examined.…”

Section: Discussionmentioning

confidence: 99%

Pretreatment with anti-VEGF therapy may exacerbate inflammation in experimental acute colitis

Chernoguz

Crawford

Vandersall

et al. 2012

Journal of Pediatric Surgery

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“…Another angiogenic factor, placental growth factor (PIGF), has also been suggested to be a marker of pathologic angiogenesis and may play a critical role in pathogenesis of UC. Accordingly, inhibition of pathologic angiogenesis by either anti-VEGF or anti-PIGF, was demonstrated to be a new approach to attenuate UC [321,322].…”

Section: Vascular Endothelial Growth Factor (Vegf)mentioning

confidence: 99%

Gut Inflammation: Current Update on Pathophysiology, Molecular Mechanism and Pharmacological Treatment Modalities

Gyires¹,

Tóth²,

Zádori

2014

CPD

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Inflammatory bowel disease (IBD) is a chronic and relapsing inflammatory condition of the gastrointestinal tract. The two main forms of IBD are Crohn's disease and ulcerative colitis. According to the recent concept the disease is caused by a combination of factors, including genetics, immune dysregulation, barrier dysfunction and the change in microbial flora. Environmental factors, such as changes in diet, antibiotic use, smoking or improved domestic hygiene (e.g. eradication of intestinal helminths) probably contribute to the development and increased prevalence of IBD. Dysregulation of mucosal immunity in IBD causes an overproduction of inflammatory cytokines which resulted in uncontrolled intestinal inflammation. Based on extensive research over the last decade, besides the conventional therapy, there are several novel pathways and specific targets, on which focus new therapeutics. New therapeutics aim 1./ to correct genetic susceptibility by stimulating NOD2 expression, TLR3 signaling or inhibition of TLR4 pathway, 2./ to restore the immune dysregulation by inhibition of pro-inflammatory cytokines (TNF-, IL-6, IL-13, IL-17, IL-18, IL-21), Th1 polarisation (IL-2, IL-12, IL-23, IFN-), T-cell activation, leukocyte adhesion, as well as by immunostimulation (GM-CSF, G-CSF) and anti-inflammatory cytokines (IL-10, IL-11, IFN--1a), 3./ to restore mucosal barrier function and stimulate mucosal healing by different growth factors, such as GH, EGF, KGF, TGF-, VEGF, 4./ to restore the normal bacterial flora by antibiotics, probiotics. However, in spite of these numerous potential targets, the true value and clinical significance of most of the new biologics and molecules are not clear yet.

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Role of anti-angiogenic factor endostatin in the pathogenesis of experimental ulcerative colitis

Cited by 23 publications

References 51 publications

Matrix Metalloproteinase-9: Its Interplay with Angiogenic Factors in Inflammatory Bowel Diseases

Matrix Metalloproteinase-9: Its Interplay with Angiogenic Factors in Inflammatory Bowel Diseases

Pretreatment with anti-VEGF therapy may exacerbate inflammation in experimental acute colitis

Gut Inflammation: Current Update on Pathophysiology, Molecular Mechanism and Pharmacological Treatment Modalities

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