blister and Hypertrophy

To examine the role of protein kinase C (PKC) and non-muscle myosin in regulation of wall tension in the hypertrophied urinary bladder.. A partial urinary outflow obstruction was induced in the mouse. Tissue strips from sham operated controls and obstructed bladders were examined in vitro with quantitative gel electrophoresis, immunohistochemistry, and in vitro force recordings.. Outlet obstruction (14-18 days) induced a significant growth of the bladder, 73 ± 6.13 mg compared to 19 ± 1 13 mg in sham operated controls. The hypertrophying bladder tissue had increased expression of non-muscle myosin B (SMemb) mainly localized to serosa and suburothelium. Direct activation of PKC with PDBu did not alter force in the control urinary bladder. In contrast, PDBu initiated a prominent and sustained contraction which had an increased sensitivity to the myosin type II inhibitor blebbistatin.. PKC activates a significant contractile response in the wall of the hypertrophying urinary bladder, possibly supported by non-muscle myosin. This contractile component is not contributing to the physiological response to muscarinic stimulation, but might be separately regulated by other, yet unknown, mechanisms.

Topics: Animals; Biomechanical Phenomena; Disease Models, Animal; Female; Heterocyclic Compounds, 4 or More Rings; Hypertrophy; In Vitro Techniques; Mice; Mice, Inbred C57BL; Muscle Contraction; Muscle, Smooth; Nonmuscle Myosin Type IIB; Phorbol 12,13-Dibutyrate; Protein Kinase C; Urinary Bladder; Urinary Bladder Neck Obstruction