ArticleLaboratory investigation; a journal of technical methods and pathology2009
Alteration of the PKC-mediated signaling pathway for smooth muscle contraction in obstruction-induced hypertrophy of the urinary bladder.
Article in Laboratory investigation; a journal of technical methods and pathology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 43 citations in OpenAlex.
- Advances in Understanding Calcium Sensitization in Gastrointestinal Smooth Muscles: Pathways, Interstitial Cells, and Disease.Journal of neurogastroenterology and motility · 2026Review
- Detrusor contractility to parasympathetic mediators is differentially altered in the compensated and decompensated states of diabetic bladder dysfunction.American journal of physiology. Renal physiology · 2019Article
- Altered detrusor contractility and voiding patterns in mice lacking the mechanosensitive TREK-1 channel.BMC urology · 2019Article
- Nerve-sparing Mid-urethral Obstruction (NeMO) in Female Small Rodents.Journal of visualized experiments : JoVE · 2017Article
- Big-conductance CaChannels (Austin, Tex.) · 2016Review
- Regulation of urinary bladder function by protein kinase C in physiology and pathophysiology.BMC urology · 2015Review
- Research Findings on Overactive Bladder.Current urology · 2015Review
- Protein kinase C modulates frequency of micturition and non-voiding contractions in the urinary bladder via neuronal and myogenic mechanisms.BMC urology · 2015Article
- The urinary bladder of spontaneously hypertensive rat demonstrates bladder hypertrophy, inflammation, and fibrosis but not hyperplasia.Life sciences · 2015Article
- Mechanical stretch upregulates proteins involved in Ca2+ sensitization in urinary bladder smooth muscle hypertrophy.American journal of physiology. Cell physiology · 2014Article
- Large-conductance voltage- and Ca2+-activated K+ channel regulation by protein kinase C in guinea pig urinary bladder smooth muscle.American journal of physiology. Cell physiology · 2014Article
- Article
- Overexpression of aquaporin-1 and caveolin-1 in the rat urinary bladder urothelium following bladder outlet obstruction.International neurourology journal · 2013Article
- Spontaneous and evoked contractions are regulated by PKC-mediated signaling in detrusor smooth muscle: involvement of BK channels.American journal of physiology. Renal physiology · 2013Article
- GATA-6 and NF-κB activate CPI-17 gene transcription and regulate Ca2+ sensitization of smooth muscle contraction.Molecular and cellular biology · 2013Article
- Endogenous inhibitor proteins that connect Ser/Thr kinases and phosphatases in cell signaling.IUBMB life · 2012Review
- Reciprocal regulation controlling the expression of CPI-17, a specific inhibitor protein for the myosin light chain phosphatase in vascular smooth muscle cells.American journal of physiology. Cell physiology · 2012Article
- Impact of partial urethral obstruction on bladder function: time-dependent changes and functional correlates of altered expression of Ca²⁺ signaling regulators.American journal of physiology. Renal physiology · 2012Article
- Adjustable passive stiffness in mouse bladder: regulated by Rho kinase and elevated following partial bladder outlet obstruction.American journal of physiology. Renal physiology · 2012Article
- Alterations in the contractile phenotype of the bladder: lessons for understanding physiological and pathological remodelling of smooth muscle.Journal of cellular and molecular medicine · 2012Review
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Normal urinary bladder function requires contraction and relaxation of the detrusor smooth muscle (DSM). The DSM undergoes compensatory hypertrophy in response to partial bladder outlet obstruction (PBOO) in both men and animal models. Following bladder hypertrophy, the bladder either retains its normal function (compensated) or becomes dysfunctional (decompensated) with increased voiding frequency and decreased void volume. We analyzed the contractile characteristics of DSM in a rabbit model of PBOO. The protein kinase C (PKC) agonist phorbol 12, 13-dibutyrate (PDBu) elicited similar levels of contraction of DSM strips from normal and compensated bladders. However, PDBu-induced contraction decreased significantly in DSM strips from decompensated bladders. The expression and activity of PKC-alpha were also lowest in decompensated bladders. The PKC-specific inhibitor bisindolylmaleimide-1 (Bis) blocked PDBu-induced contraction and PKC activity in all three groups. Moreover, the phosphorylation of the phosphoprotein inhibitor CPI-17 (a 17-kDa PKC-potentiated inhibitory protein of protein phosphatase-1) was diminished in DSM from the decompensated bladder, which would result in less inhibitory potency of CPI-17 on myosin light chain phosphatase activity and contribute to less contractility. Immunostaining revealed the colocalization of PKC and phosphorylated CPI-17 in the DSM and confirmed the decreases of these signaling proteins in the decompensated bladder. Our results show a differential PKC-mediated DSM contraction with corresponding alterations of PKC expression, activity and the phosphorylation of CPI-17. Our finding suggests a significant correlation between bladder function and PKC pathway. An impaired PKC pathway appears to be correlated with severe bladder dysfunction observed in decompensated bladders.
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