Karl-Erik Andersson led the peer-review process as the Associate Editor responsible for the paper.
Protein kinase C activation of a blebbistatin sensitive contractile component in the wall of hypertrophying mouse urinary bladder
Article first published online: 26 NOV 2013
© 2013 Wiley Periodicals, Inc.
Neurourology and Urodynamics
Volume 34, Issue 2, pages 196–202, February 2015
How to Cite
Boberg, L., Rahman, A., Poljakovic, M. and Arner, A. (2015), Protein kinase C activation of a blebbistatin sensitive contractile component in the wall of hypertrophying mouse urinary bladder. Neurourol. Urodyn., 34: 196–202. doi: 10.1002/nau.22531
Conflict of interest: none.
- Issue published online: 11 FEB 2015
- Article first published online: 26 NOV 2013
- Manuscript Accepted: 18 OCT 2013
- Manuscript Received: 1 JUL 2013
- Swedish Research council and an FP7EU (INComb)
- bladder outlet obstruction;
- non muscle myosin;
- protein kinase C
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. Neurourol. Urodynam. 34:196–202, 2015. © 2013 Wiley Periodicals, Inc.