Volume 37, Issue 4 pp. 1258-1265
ORIGINAL BASIC SCIENCE ARTICLE

A kit ligand, stem cell factor as a possible mediator inducing overactive bladder

Yasue Kubota

Corresponding Author

Yasue Kubota

Department of Clinical Physiology, Nagoya City University School of Nursing Graduate School of Nursing, Nagoya, Japan

Department of Nephro-urology, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan

Correspondence

Yasue Kubota, MD, Department of Clinical Physiology, Nagoya City University School of Nursing Graduate School of Nursing, 1, Kawasumi, Mizuho-cho, Mizuho-ku, Nagoya 467-8601, Japan.

Email: [email protected]

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Takashi Hamakawa

Takashi Hamakawa

Department of Nephro-urology, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan

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Satoshi Osaga

Satoshi Osaga

Clinical Research Management Center, Nagoya City University Hospital, Nagoya, Japan

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Atsushi Okada

Atsushi Okada

Department of Nephro-urology, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan

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Shuzo Hamamoto

Shuzo Hamamoto

Department of Nephro-urology, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan

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Noriyasu Kawai

Noriyasu Kawai

Department of Nephro-urology, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan

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Kenjiro Kohri

Kenjiro Kohri

Department of Nephro-urology, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan

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Takahiro Yasui

Takahiro Yasui

Department of Nephro-urology, Nagoya City University Graduate School of Medical Sciences, Nagoya, Japan

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First published: 07 November 2017
Citations: 4
Lori Birder led the peer-review process as the Associate Editor responsible for the paper.

Abstract

Objective

To investigate whether c-kit ligand, stem cell factor (SCF) affects the biological behavior of overactive bladder (OAB) and discuss the role of SCF as a possible mediator inducing OAB.

Materials and methods

First, we performed an immunohistochemical study to examine the localization of SCF in the guinea pig and human bladder. Next, urinary SCF levels were measured in patients with OAB and in control subjects to evaluate a potential biomarker for the diagnosis of OAB. Third, we examined the effect of SCF administration on the urinary bladder using guinea pigs to obtain additional information about SCF. The animals were administered with mouse SCF, and cystometry was performed. The following urodynamic parameters were analyzed: inter-contraction interval, maximum voiding pressure, pressure threshold, detrusor baseline pressure, and the number of non-voiding contractions.

Results

Immunohistochemical study showed that the expression of SCF was observed throughout the bladder wall, but especially in the urothelium of guinea pig and human bladder. Medians and IQRs of urinary SCF and SCF/creatinine levels in OAB patients (85.9 pg/mL [42.8, 199.0] and 1.30 [0.56, 2.71], respectively) were significantly higher than in control subjects (18.9 pg/mL [5.0, 43.6] and 0.26 [0.13, 0.43], respectively). SCF administration dose-dependently shortened the intercontraction interval and an increased number of non-voiding contractions (P < 0.05).

Conclusions

Our present data suggest that SCF produced in the urinary bladder may act as a possible mediator by binding to c-kit, which is expressed in ICC-like cells in the suburothelial and muscle layers, to control bladder function.

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