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Correlation of gene expression with bladder capacity in interstitial cystitis/bladder pain syndrome.
Colaco, Marc; Koslov, David S; Keys, Tristan; Evans, Robert J; Badlani, Gopal H; Andersson, Karl-Erik; Walker, Stephen J.
Afiliação
  • Colaco M; Wake Forest Institute for Regenerative Medicine, Wake Forest School of Medicine, Winston-Salem, North Carolina. Electronic address: mcolaco@wakehealth.edu.
  • Koslov DS; Wake Forest Institute for Regenerative Medicine, Wake Forest School of Medicine, Winston-Salem, North Carolina.
  • Keys T; Wake Forest Institute for Regenerative Medicine, Wake Forest School of Medicine, Winston-Salem, North Carolina.
  • Evans RJ; Department of Urology, Wake Forest School of Medicine, Winston-Salem, North Carolina.
  • Badlani GH; Department of Urology, Wake Forest School of Medicine, Winston-Salem, North Carolina.
  • Andersson KE; Wake Forest Institute for Regenerative Medicine, Wake Forest School of Medicine, Winston-Salem, North Carolina.
  • Walker SJ; Wake Forest Institute for Regenerative Medicine, Wake Forest School of Medicine, Winston-Salem, North Carolina.
J Urol ; 192(4): 1123-9, 2014 Oct.
Article em En | MEDLINE | ID: mdl-24840534
ABSTRACT

PURPOSE:

Interstitial cystitis and bladder pain syndrome are terms used to describe a heterogeneous chronic pelvic and bladder pain disorder. Despite its significant prevalence, our understanding of disease etiology is poor. We molecularly characterized interstitial cystitis/bladder pain syndrome and determined whether there are clinical factors that correlate with gene expression. MATERIALS AND

METHODS:

Bladder biopsies from female subjects with interstitial cystitis/bladder pain syndrome and female controls without signs of the disease were collected and divided into those with normal and low anesthetized bladder capacity, respectively. Samples then underwent RNA extraction and microarray assay. Data generated by these assays were analyzed using Omics Explorer (Qlucore, Lund, Sweden), GeneSifter® Analysis Edition 4.0 and Ingenuity® Pathway Analysis to determine similarity among samples within and between groups, and measure differentially expressed transcripts unique to each phenotype.

RESULTS:

A total of 16 subjects were included in study. Principal component analysis and unsupervised hierarchical clustering showed clear separation between gene expression in tissues from subjects with low compared to normal bladder capacity. Gene expression in tissue from patients with interstitial cystitis/bladder pain syndrome who had normal bladder capacity did not significantly differ from that in controls without interstitial cystitis/bladder pain syndrome. Pairwise analysis revealed that pathways related to inflammatory and immune response were most involved.

CONCLUSIONS:

Microarray analysis provides insight into the potential pathological condition underlying interstitial cystitis/bladder pain syndrome. This pilot study shows that patients with this disorder who have low compared to normal bladder capacity have significantly different molecular characteristics, which may reflect a difference in disease pathophysiology.
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Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Bexiga Urinária / RNA / Regulação da Expressão Gênica / Dor Pélvica / Cistite Intersticial Tipo de estudo: Etiology_studies / Observational_studies / Prevalence_studies / Prognostic_studies / Risk_factors_studies Limite: Adolescent / Adult / Aged / Aged80 / Female / Humans / Middle aged País/Região como assunto: Europa Idioma: En Revista: J Urol Ano de publicação: 2014 Tipo de documento: Article

Texto completo: 1 Coleções: 01-internacional Base de dados: MEDLINE Assunto principal: Bexiga Urinária / RNA / Regulação da Expressão Gênica / Dor Pélvica / Cistite Intersticial Tipo de estudo: Etiology_studies / Observational_studies / Prevalence_studies / Prognostic_studies / Risk_factors_studies Limite: Adolescent / Adult / Aged / Aged80 / Female / Humans / Middle aged País/Região como assunto: Europa Idioma: En Revista: J Urol Ano de publicação: 2014 Tipo de documento: Article