title: O-GlcNAc mediated glycosylation down-regulation in mice with cyclophosphamide induced cystitis.
abstract: OBJECTIVE
  Cyclophosphamide induced cystitis is an established model for the study of bladder injury and wound healing. Glycosylation is an important modification mechanism that regulates the structure and function of secreted proteins and growth factors from inflammation sites. We determined the effect of cyclophosphamide induced cystitis on O-GlcNAc mediated glycosylation in the bladder.
  
  
  METHODS
  Cystitis in WT C57BL6 mice was induced with intraperitoneal cyclophosphamide. Retrieved bladders were analyzed using histology, immunohistochemistry, reverse transcriptase-polymerase chain reaction and Western blot for glycosylation associated factors.
  
  
  RESULTS
  Acute bladder injury was seen up to 168 hours (7 days) after injection. Reverse transcriptase-polymerase chain reaction revealed down-regulation of O-GlcNAc transferase, a key enzyme in O-GlcNAc mediated glycosylation, at the 8, 48 and 168-hour time points. Also, the glycosidase menangioma expressed antigen 5 was up-regulated at similar time points. Western blot analysis revealed decreased glycosylated protein during cyclophosphamide induced inflammation.
  
  
  CONCLUSIONS
  To our knowledge we report the first study of alterations in O-GlcNAc mediated glycosylation activity in bladders with cyclophosphamide induced cystitis. Glycosylation may have a significant role in the bladder wound healing process. Future studies of the glycosylation signaling pathways in the bladder would assist in future potential therapy for bladder inflammatory disease and cancer by elucidating pathways that guide bladder development and wound healing.
authors.affiliation: Developmental Biology, Regenerative Medicine and Surgery Program, Saban Research Institute, Children's Hospital Los Angeles, Los Angeles, California, USA.
authors.forename: Seyung
authors.initials: S
authors.lastname: Chung
authors.forename: Dae-Ook
authors.initials: DO
authors.lastname: Kang
authors.forename: Jonathan
authors.initials: J
authors.lastname: Yamzon
authors.forename: David
authors.initials: D
authors.lastname: Warburton
authors.forename: Chester J
authors.initials: CJ
authors.lastname: Koh
mesh_terms: D000818:Animals; D003520:Cyclophosphamide / Q000008:administration & dosage; D003556:Cystitis / Q000139:chemically induced / Q000201:enzymology*; D015536:Down-Regulation / Q000502:physiology*; D006031:Glycosylation; D051379:Mice; D017351:N-Acetylglucosaminyltransferases / Q000502:physiology*
chemical_list: D003520:Cyclophosphamide; D017351:N-Acetylglucosaminyltransferases; C063057:UDP-N-acetylglucosamine-peptide beta-N-acetylglucosaminyltransferase