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.
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.