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Does diabetes affect the distribution and number of interstitial cells and neuronal tissue in the ureter, bladder, prostate, and urethra of humans?

Canda AE, Dogan H, Kandemir O, Atmaca AF, Akbulut Z, Balbay MD - Cent European J Urol (2014)

Bottom Line: The mean number of c-kit (+) ICs in bladder lamina propria was significantly decreased in diabetics (32.40 ±12.96 versus 57.18 ±25.37, p = 0.036).The mean number of ICs in the detrusor muscle was significantly decreased in diabetics (40.50 ±16.79 versus 64.55 ±22.08, p = 0.013).Between the groups, no significant differences were detected regarding the number of ICs at the level of the ureter, urethra, and prostate.

View Article: PubMed Central - PubMed

Affiliation: Yildirim Beyazit University, School of Medicine, Ankara Ataturk Training & Research Hospital, Department of Urology, Ankara, Turkey.

ABSTRACT

Introduction: The aim of this study was to investigate and compare the distribution and number of interstitial cells (ICs) and neuronal tissue in the ureter, bladder, prostate, and urethra of human patients with and without diabetes.

Material and methods: Human tissue was obtained from patients who had undergone radical cystectomy for bladder cancer (10 diabetic and 11 non-diabetic males). Interstitial cells were stained immunohistochemically with anti-human CD117 (c-kit) rabbit polyclonal antibody, Vimentin, and Connexin-43. Neural tissue was stained with synaptophysin. The number of ICs and neurons was evaluated and compared between the groups (diabetic versus non-diabetic).

Results: The mean number of c-kit (+) ICs in bladder lamina propria was significantly decreased in diabetics (32.40 ±12.96 versus 57.18 ±25.37, p = 0.036). The mean number of ICs in the detrusor muscle was significantly decreased in diabetics (40.50 ±16.79 versus 64.55 ±22.08, p = 0.013). Between the groups, no significant differences were detected regarding the number of ICs at the level of the ureter, urethra, and prostate. No significant differences were detected regarding the number of nerves in the ureter, bladder, prostate, and urethra of both groups.

Conclusions: The number of ICs may be decreased in the lamina propria and detrusor muscle of the human bladder in diabetes. This can be an underlying cause of lower urinary tract (LUT) dysfunction in diabetics. Research into the development of drugs targeting or stimulating IC function in order to prevent diabetic LUT dysfunction is warranted.

No MeSH data available.


Related in: MedlinePlus

Light microscopic appearance of nerves stained with synaptophysin in the urinary bladder of a non–diabetic patient (x400). Arrows indicate some of the nerve fibers.
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Figure 0003: Light microscopic appearance of nerves stained with synaptophysin in the urinary bladder of a non–diabetic patient (x400). Arrows indicate some of the nerve fibers.

Mentions: Nerves detected immunohistochemically by synaptophysin staining were detected microscopically by antibodies targeting synaptophysin both in diabetic and non–diabetic urinary tract tissues (Figure 3).


Does diabetes affect the distribution and number of interstitial cells and neuronal tissue in the ureter, bladder, prostate, and urethra of humans?

Canda AE, Dogan H, Kandemir O, Atmaca AF, Akbulut Z, Balbay MD - Cent European J Urol (2014)

Light microscopic appearance of nerves stained with synaptophysin in the urinary bladder of a non–diabetic patient (x400). Arrows indicate some of the nerve fibers.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4310884&req=5

Figure 0003: Light microscopic appearance of nerves stained with synaptophysin in the urinary bladder of a non–diabetic patient (x400). Arrows indicate some of the nerve fibers.
Mentions: Nerves detected immunohistochemically by synaptophysin staining were detected microscopically by antibodies targeting synaptophysin both in diabetic and non–diabetic urinary tract tissues (Figure 3).

Bottom Line: The mean number of c-kit (+) ICs in bladder lamina propria was significantly decreased in diabetics (32.40 ±12.96 versus 57.18 ±25.37, p = 0.036).The mean number of ICs in the detrusor muscle was significantly decreased in diabetics (40.50 ±16.79 versus 64.55 ±22.08, p = 0.013).Between the groups, no significant differences were detected regarding the number of ICs at the level of the ureter, urethra, and prostate.

View Article: PubMed Central - PubMed

Affiliation: Yildirim Beyazit University, School of Medicine, Ankara Ataturk Training & Research Hospital, Department of Urology, Ankara, Turkey.

ABSTRACT

Introduction: The aim of this study was to investigate and compare the distribution and number of interstitial cells (ICs) and neuronal tissue in the ureter, bladder, prostate, and urethra of human patients with and without diabetes.

Material and methods: Human tissue was obtained from patients who had undergone radical cystectomy for bladder cancer (10 diabetic and 11 non-diabetic males). Interstitial cells were stained immunohistochemically with anti-human CD117 (c-kit) rabbit polyclonal antibody, Vimentin, and Connexin-43. Neural tissue was stained with synaptophysin. The number of ICs and neurons was evaluated and compared between the groups (diabetic versus non-diabetic).

Results: The mean number of c-kit (+) ICs in bladder lamina propria was significantly decreased in diabetics (32.40 ±12.96 versus 57.18 ±25.37, p = 0.036). The mean number of ICs in the detrusor muscle was significantly decreased in diabetics (40.50 ±16.79 versus 64.55 ±22.08, p = 0.013). Between the groups, no significant differences were detected regarding the number of ICs at the level of the ureter, urethra, and prostate. No significant differences were detected regarding the number of nerves in the ureter, bladder, prostate, and urethra of both groups.

Conclusions: The number of ICs may be decreased in the lamina propria and detrusor muscle of the human bladder in diabetes. This can be an underlying cause of lower urinary tract (LUT) dysfunction in diabetics. Research into the development of drugs targeting or stimulating IC function in order to prevent diabetic LUT dysfunction is warranted.

No MeSH data available.


Related in: MedlinePlus