Alterations in Extracellular Matrix Gene Expression in Normal Versus Non-Compliant Human Bladders
Congenital or acquired obstruction of the urinary bladder can result in a stiff-walled, fibrotic organ characterized by trabeculation, low volume capacity at high pressures, and, in some cases, the occurrence of uninhibited contractions of the detrusor muscle cells. This fibrotic response is likely characterized by an alteration in the quantity and type of connective tissue (collagens and elastin) and, possibly, in the arrangement of these matrix components with one another and with the detrusor smooth muscle cells. The bladder wall becomes thickened, and the smooth muscle fascicles become infiltrated with connective tissue (2,3,4,5,6). As a result, the bladder loses compliance. This decreased compliance has been observed in up to 50% of patients suffering from spinal cord injury resulting from sacral nerve damage and 70% of myelomeningocele patients (1). Initial studies in our laboratory were carried out to characterize the connective tissue changes in non-compliant human bladders from a pediatric patient population composed of children with neurogenic, non-compliant bladders secondary to myelomeningocele. Results of these studies showed that the connective tissue infiltration within the detrusor muscle fascicles in the neurogenic bladders was specific for type III collagen (7).
KeywordsCollagenase Guanidinium Pyelonephritis Glyceraldehyde
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