PDGF May Play a Role in Pressure Induced Bladderwall Hyperplasia and Acts in a Paracrine Way
Purpose In previous experiments w+e have shown a proliferative effect of platelet derived growth factor (PDGF) on smooth muscle cells (SMC) of the human bladder. We also could show a gene expression of its receptor (PDGFR) after short-term mechanical load of SMC supporting a regulatory role for PDGF in terms of pressure-induced hyperplasia. In these experiments we focused on urothelial cells (UC) as a possible site of PDGF-synthesis. Material and Methods SMC (detrusor muscle) were taken from patients in the course of an ureteral reimplant procedure. UC were collected by cystoscopic bladder washing. Primary cell cultures were created. In select experiments SMC and UC were treated with predefined pressure for 1 hour. Gene expression for PDGF and PDGFR was measured by real-time PCR. At protein level we performed immunohistochemical staining and western-blotting. Results After mechanical load SMC showed a significant increase in gene expression of PDGFR (alpha and beta) with different pressure patterns. PDGF itself was not expressed in SMC. In contrast, UC showed no expression of PDGFR but of PDGF. However, PDGF expression could not be increased by different pressure patterns. Conclusions Gene expression of PDGFR after short-term mechanical load of SMC of the bladder supports a regulatory role for PDGF in terms of pressure-induced hyperplasia of the human bladder. Since we could demonstrate UC as a site of PDGF-sythesis, the growth factor may act on a paracrine way. Further experiments will focus on PDGFR autophosphorylation under pressure conditions.