RGD Reference Report - Angiogenic remodeling in pediatric eosinophilic esophagitis is associated with increased levels of VEGFA, angiogenin, IL-8 and activation of the TNF-alpha-NFkappaB pathway. - Rat Genome Database

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Angiogenic remodeling in pediatric eosinophilic esophagitis is associated with increased levels of VEGFA, angiogenin, IL-8 and activation of the TNF-alpha-NFkappaB pathway.

Authors: Persad, R  Huynh, HQ  Hao, L  Ha, JR  Sergi, C  Srivastava, R  Persad, S 
Citation: Persad R, etal., J Pediatr Gastroenterol Nutr. 2012 Feb 10.
RGD ID: 6771318
Pubmed: PMID:22331014   (View Abstract at PubMed)
DOI: DOI:10.1097/MPG.0b013e31824b6391   (Journal Full-text)

ABSTRACT: Eosinophilic Esophagitis (EoE) is a clinicopathologic diagnosis characterized by inflammation and infiltration of eosinophils at the esophageal mucosa. The underlying etiology of EoE remains elusive. Inflammatory diseases, such as asthma, are associated with structural remodeling of the airways, which includes angiogenesis. We compared the angiogenic profile of the esophageal mucosa of pediatric patients presenting with EoE relative to control. In addition, we investigated putative mechanism(s) that may be involved in the pathogenesis of the inflammatory angiogenic response observed in EoE. METHODS & RESULTS:: Endoscopically obtained biopsy samples from 18 EoE and 18 control pediatric patients were analyzed for angiogenic markers (CD-31, vWF, VCAM-1) and tissue levels of angiogenic factors (VEGFA, VEGF R2, angiogenin and IL-8). Samples from EoE patients exhibited higher levels of vWF, CD31 and VCAM-1 suggestive of neovascularization and an activated endothelium. Moreover, EoE biopsies showed greater levels of the angiogenesis promoters, VEGFA, angiogenin and IL-8. Interestingly, there were greater cellular levels of TNF-alpha in EoE samples compared to control. Further, there were higher nuclear levels of p50 and p65 subunits of NFkappaB and lower cellular levels of the inhibitor of NFkappaB, IkappaB-alpha, in EoE samples compared to control. CONCLUSIONS:: We demonstrate increased angiogenesis in the esophageal mucosa of pediatric patients with EoE. The data also provided evidence that the angiogenic factors VEGFA, angiogenin and IL-8 were prominently involved in promoting angiogenic remodeling. Furthermore, activation of the TNF-alpha-NF-kappaB pathway, at least partially, played a role in mediating and triggering the observed inflammatory response-induced angiogenesis.



RGD Manual Disease Annotations    Click to see Annotation Detail View

  
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
ANGHumaneosinophilic esophagitis  IEP  RGD 
AngMouseeosinophilic esophagitis  ISOANG (Homo sapiens) RGD 
AngRateosinophilic esophagitis  ISOANG (Homo sapiens) RGD 
PECAM1Humaneosinophilic esophagitis  IEP protein:increased expression:esophagus (human)RGD 
Pecam1Rateosinophilic esophagitis  ISOPECAM1 (Homo sapiens)protein:increased expression:esophagus (human)RGD 
Pecam1Mouseeosinophilic esophagitis  ISOPECAM1 (Homo sapiens)protein:increased expression:esophagus (human)RGD 

Objects Annotated

Genes (Rattus norvegicus)
Ang  (angiogenin)
Pecam1  (platelet and endothelial cell adhesion molecule 1)

Genes (Mus musculus)
Ang  (angiogenin, ribonuclease, RNase A family, 5)
Pecam1  (platelet/endothelial cell adhesion molecule 1)

Genes (Homo sapiens)
ANG  (angiogenin)
PECAM1  (platelet and endothelial cell adhesion molecule 1)


Additional Information