Peripheral blood mononuclear cell gene array profiles in female patients with involuntary bladder contractions

ipheral blood mononuclear cell gene array profiles in female patients with involuntary bladder contractions Original Research (3046) Total Article Views Authors: Cheung W, Bluth MJ, Khan S, Johns C, Bluth MH Published Date June 2011 Volume 2011:1 Pages 3 - 7 DOI: http://dx.doi.org/10.2147/AGG.S17640 Wellman Cheung1, Mark J Bluth1, Sohail Khan2, Christopher Johns2, Martin H Bluth3 1State University of New York Downstate Medical Center, Brooklyn, NY, USA; 2Cold Spring Harbor Laboratory – Microarray Shared Resource, Cold Spring Harbor, NY, USA; 3Wayne State University School of Medicine, Detroit, MI, USA Background: Patients with urgency represent a group of incontinence sufferers whose diagnosis remains difficult to establish. Urodynamic testing demonstrating involuntary bladder contraction provides objective confirmation but represents an invasive approach. We have previously demonstrated that peripheral blood mononuclear cells (PBMC) can provide a reporter function in solid organ disease toward biomarker discovery. Here we investigated the utility of using PBMC as marker for patients with confirmed involuntary bladder contraction. Methods: Fifteen female patients were evaluated for involuntary bladder contractions and stress urinary incontinence as demonstrated by urodynamics and also assessed for pelvic prolapse, stress incontinence by history, bladder neck dysfunction, and bladder capacity. PBMC were obtained from patients’ whole blood, and RNA was subjected to microarray gene chip analysis. Results: Microarray analysis revealed that eleven genes were differentially regulated (five upregulated and six downregulated). Of these, PGRMC1 (progesterone receptor membrane component 1), EIF2S3 (eukaryotic initiation factor), C3AR1 (complement receptor), and three unknown genes were downregulated. Upregulated genes included MYOM2 (myomesin M-protein), a cytoskeletal protein; KTN1 (kinectin); and AAK 1 (AP2 associated kinase). Conclusions: Microarray analysis revealed many genes that were differentially regulated in PBMC from patients with involuntary detrusor contractions. These genes may be important in regulating structural integrity of bladder and supporting tissues. These data suggest that PBMC can provide a reporter function for patients with involuntary bladder contractions and may serve toward biomarker discovery for novel diagnostic markers and/or the ability to monitor response to therapy.