title: Genome-based expression profiles as a single standardized microarray platform for the diagnosis of bladder pain syndrome/interstitial cystitis: an array of 139 genes model.
abstract: OBJECTIVE
  The aim of the study was to investigate the molecular signatures underlying bladder pain syndrome/interstitial cystitis (BPS/IC) using cDNA microarray.
  
  
  METHODS
  Microarray gene expression profiles were [corrected] studied in a matched case-control study [corrected] by using a system of conditional regression modeling.
  
  
  RESULTS
  The main [corrected] findings are summarized as follows: Firstly, a "139-gene" model was discovered to contain high expressions of bladder epithelium, which feature in BPS/IC. Secondly, complex metabolic reactions, including carbohydrate, lipid, cofactors, vitamins, xenobiotics, nucleotide, and amino acid metabolisms, were [corrected] found to have a strong relationship with bladder smooth muscle contraction through IC status. Thirdly, we [corrected] found the transcriptional regulations of IC-induced bladder smooth muscle contraction status, including the level of contractile force, tissue homeostasis, energy homeostasis, and the development of the [corrected] nervous system. In addition, our study suggested the mast-cell activation mediated by the high-affinity receptor of Fc epsilon [corrected] RI triggering allergic inflammation through IC status. Such genetic changes, jointly termed "bladder remodeling," [corrected] can constitute an important long-term consequence of BPS/IC. [corrected].
  
  
  CONCLUSIONS
  The success of this innovation has supported the use of microarray-based expression profiling as a single standardized platform for diagnosis of PBS/IC and offers [corrected] drug discovery.
authors.affiliation: Department of Obstetrics and Gynecology, Chang Gung Memorial Hospital and University of Chang Gung School of Medicine, Taoyuan 333, Taiwan.
authors.forename: Ling-Hong
authors.initials: LH
authors.lastname: Tseng
authors.forename: Ilene
authors.initials: I
authors.lastname: Chen
authors.forename: Ming-Yang
authors.initials: MY
authors.lastname: Chen
authors.forename: Chyi-Long
authors.initials: CL
authors.lastname: Lee
authors.forename: Yi-Hao
authors.initials: YH
authors.lastname: Lin
authors.forename: L Keith
authors.initials: LK
authors.lastname: Lloyd
mesh_terms: D000199:Actins / Q000235:genetics / Q000378:metabolism; D054392:Adipokines / Q000235:genetics / Q000378:metabolism; D000596:Amino Acids / Q000378:metabolism; D017209:Apoptosis / Q000235:genetics; D050260:Carbohydrate Metabolism / Q000235:genetics; D016022:Case-Control Studies; D002478:Cells, Cultured; D018856:Cystitis, Interstitial / Q000175:diagnosis* / Q000235:genetics*; D016207:Cytokines / Q000235:genetics; D018076:DNA, Complementary; D004847:Epithelial Cells; D005260:Female; D020869:Gene Expression Profiling; D006706:Homeostasis / Q000235:genetics; D006801:Humans; D050356:Lipid Metabolism / Q000235:genetics; D016015:Logistic Models; D020935:MAP Kinase Signaling System / Q000235:genetics; D009119:Muscle Contraction / Q000235:genetics*; D009130:Muscle, Smooth / Q000294:innervation / Q000378:metabolism*; D020411:Oligonucleotide Array Sequence Analysis; D047492:Peroxisome Proliferator-Activated Receptors / Q000235:genetics / Q000378:metabolism; D059467:Transcriptome; D016212:Transforming Growth Factor beta / Q000235:genetics / Q000378:metabolism; D019459:Urothelium
chemical_list: D000199:Actins; D054392:Adipokines; D000596:Amino Acids; D016207:Cytokines; D018076:DNA, Complementary; D047492:Peroxisome Proliferator-Activated Receptors; D016212:Transforming Growth Factor beta