Introduction and hypothesis: 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.