title: Proteomic Analysis in Esophageal Eosinophilia Reveals Differential Galectin-3 Expression and S-Nitrosylation.
abstract: OBJECTIVE
  Esophageal eosinophilia (EE) can be caused by gastroesophageal reflux disease (GERD), proton-pump inhibitor-responsive EE (PPI-REE) or eosinophilic esophagitis (EoE). This study quantified protein expression and S-nitrosylation (SNO) post-translational modifications in EE to elucidate potential disease biomarkers.
  
  
  METHODS
  Proximal and distal esophageal (DE) biopsy proteins in patients with EE and in controls were assayed for protein content and fluorescence-labeled with and without ascorbate treatment. Protein SNO was determined, and selected protein spots were identified by matrix-assisted laser desorption ionization time-of-flight/mass spectrometry. Western blot and ingenuity pathway analysis were performed.
  
  
  RESULTS
  Ninety-one of 648 proteins showed differential expression. There were significantly altered levels of abundance for 11 proximal and 14 DE proteins. Hierarchal clustering revealed differential SNO in inflamed tissues, indicating reactive nitrogen/oxygen species involvement. Galectin-3 was upregulated in both proximal (p < 0.04) and distal (p < 0.004) esophageal EE biopsies compared to controls. In distal EE samples, galectin-3 was significantly S-nitrosylated (p < 0.004). Principal component analysis revealed sample group discrimination distally.
  
  
  CONCLUSIONS
  Proteomic analysis in EE esophageal mucosa revealed a distinct abundance and nitrosylation profile, most prominently in distal biopsies. Galectin-3 was upregulated in expression and SNO, which may indicate its potential role in mucosal inflammation. These results call for more studies to be performed to investigate the role of galectin-3 in GERD, PPI-REE and EoE.
authors.affiliation: Section of Immunology, Allergy and Rheumatology, Department of Pediatrics, Baylor College of Medicine, Houston, Tex., USA.
authors.forename: Carla M
authors.initials: CM
authors.lastname: Davis
authors.forename: Girish
authors.initials: G
authors.lastname: Hiremath
authors.forename: John E
authors.initials: JE
authors.lastname: Wiktorowicz
authors.forename: Kizhake V
authors.initials: KV
authors.lastname: Soman
authors.forename: Christof
authors.initials: C
authors.lastname: Straub
authors.forename: Christina
authors.initials: C
authors.lastname: Nance
authors.forename: Norma
authors.initials: N
authors.lastname: Quintanilla
authors.forename: Konrad
authors.initials: K
authors.lastname: Pazdrak
authors.forename: Kalpesh
authors.initials: K
authors.lastname: Thakkar
authors.forename: Anthony P
authors.initials: AP
authors.lastname: Olive
authors.forename: Alexander
authors.initials: A
authors.lastname: Kurosky
mesh_terms: D000293:Adolescent; D015415:Biomarkers / Q000378:metabolism; D001706:Biopsy; D001798:Blood Proteins; D002648:Child; D002675:Child, Preschool; D004802:Eosinophilia / Q000378:metabolism* / Q000473:pathology; D057765:Eosinophilic Esophagitis / Q000188:drug therapy / Q000378:metabolism* / Q000473:pathology; D000071041:Esophageal Mucosa / Q000378:metabolism* / Q000473:pathology; D037502:Galectin 3 / Q000378:metabolism*; D037161:Galectins; D005764:Gastroesophageal Reflux / Q000188:drug therapy / Q000378:metabolism* / Q000473:pathology; D006801:Humans; D009569:Nitric Oxide / Q000378:metabolism; D015538:Nitrosation; D011499:Protein Processing, Post-Translational; D040901:Proteomics; D054328:Proton Pump Inhibitors / Q000627:therapeutic use; D019032:Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization; D053719:Tandem Mass Spectrometry
chemical_list: D015415:Biomarkers; D001798:Blood Proteins; D037502:Galectin 3; D037161:Galectins; C428445:LGALS3 protein, human; D054328:Proton Pump Inhibitors; D009569:Nitric Oxide