Get access

Protein kinase C activation of a blebbistatin sensitive contractile component in the wall of hypertrophying mouse urinary bladder

Authors

  • Lena Boberg,

    1. Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden
    Search for more papers by this author
  • Awahan Rahman,

    1. Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden
    Search for more papers by this author
  • Mirjana Poljakovic,

    1. Department of Molecular Medicine and Surgery, Urology laboratory, Karolinska Institutet, Stockholm, Sweden
    2. Department of Urology, Karolinska University Hospital Solna, Stockholm, Sweden
    Search for more papers by this author
  • Anders Arner

    Corresponding author
    1. Department of Physiology and Pharmacology, Karolinska Institutet, Stockholm, Sweden
    • Correspondence to: Anders Arner, M.D., Ph.D, Department of Physiology and Pharmacology, Karolinska Institutet, v Eulers v 8, SE 171 77 Stockholm, Sweden. E-mail: anders.arner@ki.se

    Search for more papers by this author

  • Karl-Erik Andersson led the peer-review process as the Associate Editor responsible for the paper.
  • Conflict of interest: none.

Abstract

Aim

To examine the role of protein kinase C (PKC) and non-muscle myosin in regulation of wall tension in the hypertrophied urinary bladder.

Methods

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.

Results

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.

Conclusions

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.

Ancillary