Abstract
Aim
To explore the potential molecular mechanisms underlying experimental neurogenic bladder dysfunction.
Methods
With the aid of Affymetrix GeneChip Rat Genome U34A arrays, we examined microarray gene expression profiles in bladder wall tissue from female Sprague–Dawley rats within the first 3 weeks following spinal cord injury. Gene transcripts expressed in rat bladder wall tissue at 3 days, 7 days, and 3 weeks following spinal cord injury were compared to normal rat bladder wall tissue.
Results
The Mahalanobis distance in hierarchical cluster analysis revealed a 48‐gene model, which contained high expressions in rat bladder wall tissue at 3 days, 7 days, and 3 weeks following spinal cord injury. According to gene ontology, plausible molecular alterations in rat bladder wall tissue following spinal cord injury include: (1) the release of nerve growth factor (NGF) and transforming growth factor beta 1 (Tgfb1) (2) the secretion of histamine from mast cells, (3) the occurrence of blood coagulation, (4) the occurrence of N‐terminal protein myristoylation, and (5) Axon guidance mediated by Ena/Vasodilator‐stimulated phosphoprotein (Ena/VASP) promotes reestablishment of the bladder reflex following spinal cord injury. Such changes, jointly termed “bladder remodeling,” can constitute an important long‐term consequence of neurogenic bladder dysfunction.
Conclusion
The success of this innovation has supported the use of microarray‐based expression profiling as a commonplace platform for the pathogenesis and therapeutic interventions of experimental neurogenic bladder dysfunction. dysfunction. Neurourol. Urodynam. 29:1439–1443, 2010. © 2009 Wiley‐Liss, Inc.