Mp09-16 Pharmacological Inhibition of the Nlrp3 Inflammasome Prevents Bladder Decompensation in a Rat Model of Chronic Bladder Outlet Obstruction

Abstract

A chromosome analysis of the cells revealed a normal 46XY diploid karyotype. hBS11 cells expressed smooth muscle differentiation marker proteins, including MYH11, a-SMA, g-SMA, and calponin. The connexin 43 signals were also detected as spotty signals on the surface of hBS11 cells. M2 and M3 receptors expressed in differentiated hBS11 cells. Both the cholinergic receptor agonist calbachol and a high concentration of extracellular potassium increased intracellular calcium in differentiated hBS11 cells. Differentiated hBS11 cells stimulated by calcium ionophore (A23187) exhibited contractility.CONCLUSIONS: The present study demonstrates that the hBS11 cell maintains plasticity of the differentiation that a smooth muscle cell originally has. Immortalized hBS11 cell provides useful analytical system for elucidation of the pathophysiological mechanism of lower urinary tract dysfunction and the development of the new treatment options, in addition to the elucidation of molecular differentiation mechanism, reproduction mechanism, and the function control mechanism of the smooth muscle cell.