Altered angiogenic balance in ulcerative colitis: A key to impaired healing?

Sándor, Zsolt; Deng, Xiaoming; Khomenko, Tetyana; Tarnawski, Andrzej S.; Szabó, Sándor

doi:10.1016/j.bbrc.2006.09.021

Cited by 37 publications

(52 citation statements)

References 32 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…A dysfunctional intestinal vasculature has been implicated in the maintenance of colitis, with studies noting an increase in vascularization around sites of inflammation (Sandor et al, 2006;Danese, 2007). Thus, reduced intestinal vascularization was unexpected in the context of findings in mammalian systems and our observation of increased cellular proliferation in the gut.…”

Section: Discussionmentioning

confidence: 72%

A chemical enterocolitis model in zebrafish larvae that is dependent on microbiota and responsive to pharmacological agents

Oehlers

Flores

Okuda

et al. 2010

Developmental Dynamics

120

168

View full text Add to dashboard Cite

Inflammatory bowel disease (IBD) results from dysfunctional interactions between the intestinal immune system and microbiota, influenced by host genetic susceptibility. Because a key feature of the pathology is intestinal epithelial damage, potential disease factors have been traditionally analyzed within the background of chemical colitis models in mice. The zebrafish has greatly complemented the mouse for modeling aspects of disease processes, with an advantage for high content drug screens. Larval zebrafish exposed to the haptenizing agent trinitrobenzene sulfonic acid (TNBS) displayed impaired intestinal homeostasis and inflammation reminiscent of human IBD. There was a marked induction of pro-inflammatory cytokines, the degradative enzyme mmp9 and leukocytosis. Enterocolitis was dependent on microbiota and Toll-like receptor signaling, that can be ameliorated by antibiotic and anti-inflammatory drug treatments. This system will be useful to rapidly interrogate in vivo the biological significance of the IBD candidate genes so far identified and to carry out pharmacological modifier screens. Developmental Dynamics 240:288-298,

show abstract

Section: Discussionmentioning

confidence: 72%

A chemical enterocolitis model in zebrafish larvae that is dependent on microbiota and responsive to pharmacological agents

Oehlers

Flores

Okuda

et al. 2010

Developmental Dynamics

120

168

View full text Add to dashboard Cite

show abstract

“…Evidence indicates that some of the upregulated angiogenic factors involved in colitis may prevent the maturation of vessels, contributing to the pathological nature of this angiogenesis. Recently, angiostatin and endostatin have been shown to be involved during IBD, and it is possible that they are involved in prevention of vessel maturation and ulcer healing (131). For example, angiostatin production by MMPs has been shown to inhibit vessel maturation (36), and inhibition of pericyte stabilization of the vasculature results in endothelial cell hyperplasia and abnormal formation (59).…”

Section: Involvement Of the Microvasculature In Ibdmentioning

confidence: 99%

“…Angiostatin is known to be antiangiogenic and involved in mediating vascularization during colitis as discussed under Inflammatory Mediators. Additionally, endostatin has been observed to be upregulated in TNBS colitis and in UC (131). Endostatin is a proteolytic fragment of collagen type XVIII and is shown to inhibit angiogenesis through antimigratory and antiproliferative mechanisms (165).…”

Section: Antiangiogenic Gene Expression and Therapeutics In Ibd And Ementioning

confidence: 99%

“…Endostatin is a proteolytic fragment of collagen type XVIII and is shown to inhibit angiogenesis through antimigratory and antiproliferative mechanisms (165). In the TNBS model this upregulation occurs at 6 h; however, in the DSS model endostatin and angiostatin are not upregulated upon completion of the 6-day model, suggesting a temporal response for these molecules (31,131). The upregulation of these and other antiangiogenic mediators underscores the complexity of the differential angiogenic response during experimental colitis and IBD and warrants further investigation to determine its relationship.…”

Section: Antiangiogenic Gene Expression and Therapeutics In Ibd And Ementioning

confidence: 99%

“…It has been suggested that the angiogenic components of these diseases contribute to and exacerbate disease conditions (26, 31). Recent findings, both clinical and experimental, indicate that angiogenesis also plays a crucial role in the inflammatory bowel diseases (IBD), consisting of Crohn's disease (CD) and ulcerative colitis (UC) (31,37,58,131,155). Development of new vasculature during chronic inflammation may play a negative "pathological" role by contributing to increased inflammatory responses due to dysfunctional new vessel architecture and increases in the recruitment of inflammatory cell types.…”

mentioning

confidence: 99%

See 2 more Smart Citations

Pathogenic angiogenesis in IBD and experimental colitis: new ideas and therapeutic avenues

Chidlow

Shukla²,

Grisham³

et al. 2007

American Journal of Physiology-Gastrointestinal and Liver Physi

144

114

View full text Add to dashboard Cite

Chidlow JH Jr, Shukla D, Grisham MB, Kevil CG. Pathogenic angiogenesis in IBD and experimental colitis: new ideas and therapeutic avenues. Am J Physiol Gastrointest Liver Physiol 293: G5-G18, 2007. First published April 26, 2007; doi:10.1152/ajpgi.00107.2007.-Angiogenesis is now understood to play a major role in the pathology of chronic inflammatory diseases and is indicated to exacerbate disease pathology. Recent evidence shows that angiogenesis is crucial during inflammatory bowel disease (IBD) and in experimental models of colitis. Examination of the relationship between angiogenesis and inflammation in experimental colitis shows that initiating factors for these responses simultaneously increase as disease progresses and correlate in magnitude. Recent studies show that inhibition of the inflammatory response attenuates angiogenesis to a similar degree and, importantly, that inhibition of angiogenesis does the same to inflammation. Recent data provide evidence that differential regulation of the angiogenic mediators involved in IBD-associated chronic inflammation is the root of this pathological angiogenesis. Many factors are involved in this phenomenon, including growth factors/cytokines, chemokines, adhesion molecules, integrins, matrix-associated molecules, and signaling targets. These factors are produced by various vascular, inflammatory, and immune cell types that are involved in IBD pathology. Moreover, recent studies provide evidence that antiangiogenic therapy is a novel and effective approach for IBD treatment. Here we review the role of pathological angiogenesis during IBD and experimental colitis and discuss the therapeutic avenues this recent knowledge has revealed. inflammation; T cells; growth factors; adhesion molecules; antiangiogenesis ANGIOGENESIS PLAYS AN IMPORTANT role in many chronic inflammatory diseases including but not limited to diabetic retinopathy, atherosclerosis, rheumatoid arthritis, hypercholesterolemia, and psoriasis. It has been suggested that the angiogenic components of these diseases contribute to and exacerbate disease conditions (26, 31). Recent findings, both clinical and experimental, indicate that angiogenesis also plays a crucial role in the inflammatory bowel diseases (IBD), consisting of Crohn's disease (CD) and ulcerative colitis (UC) (31,37,58,131,155). Development of new vasculature during chronic inflammation may play a negative "pathological" role by contributing to increased inflammatory responses due to dysfunctional new vessel architecture and increases in the recruitment of inflammatory cell types. Importantly, recent data have shown that angiogenic inhibition during chronic inflammatory diseases attenuates further inflammation and disease pathology (31, 37, 51). As such, expanding our knowledge of how pathological angiogenesis occurs during IBD will further our ability to treat patients with these diseases. IBD PathogenesisCD and UC are idiopathic inflammatory disorders of the intestine and/or colon in which patients suffer from rectal bleeding, severe...

show abstract

Angiogenin, angiopoietin-1, angiopoietin-2, and endostatin serum levels in inflammatory bowel disease

Oikonomou

Kapsoritakis

Kapsoritaki

et al. 2011

Inflammatory Bowel Diseases

View full text Add to dashboard Cite

show abstract

Altered angiogenic balance in ulcerative colitis: A key to impaired healing?

Cited by 37 publications

References 32 publications

A chemical enterocolitis model in zebrafish larvae that is dependent on microbiota and responsive to pharmacological agents

A chemical enterocolitis model in zebrafish larvae that is dependent on microbiota and responsive to pharmacological agents

Pathogenic angiogenesis in IBD and experimental colitis: new ideas and therapeutic avenues

Angiogenin, angiopoietin-1, angiopoietin-2, and endostatin serum levels in inflammatory bowel disease

Contact Info

Product

Resources

About