Decreased cellular membrane expression of gap junctional protein, connexin 43, in rat detrusor muscle with chronic partial bladder outlet obstruction

Mori, Kenichi; Noguchi, Mitsuru; Matsuo, M.; Nomata, Koichiro; Suematsu, Takashi; Kanetake, Hiroshi

doi:10.1016/j.urology.2005.01.043

Cited by 22 publications

(22 citation statements)

References 20 publications

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“…In the normal bladder, connexin 43 is mainly located in interstitial cells around muscle bundles (34). However, in overactive bladders under obstruction, connexin 43 is upregulated in the detrusor smooth muscle, as reported by Christ and colleagues and other groups (5,11,23,25), strongly suggesting a correlation between them. In contrast, connexin 45 is reported to locate predominantly between smooth muscle cells (18,34), but the expression level remains unchanged in obstructed bladders (18,34).…”

mentioning

confidence: 65%

Basic fibroblast growth factor causes urinary bladder overactivity through gap junction generation in the smooth muscle

Imamura¹,

Negoro²,

Kanematsu³

et al. 2009

American Journal of Physiology-Renal Physiology

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Overactive bladder is a highly prevalent clinical condition that is often caused by bladder outlet obstruction (BOO). Increased coupling of bladder smooth muscle cells (BSMC) via gap junctions has been hypothesized as a mechanism for myogenic bladder overactivity in BOO, although little is known about the regulatory system underlying such changes. Here, we report the involvement of basic fibroblast growth factor (bFGF) and connexin 43, a bladder gap junction protein, in bladder overactivity. BOO created by urethral constriction in rats resulted in elevated bFGF and connexin 43 levels in the bladder urothelium and muscle layer, respectively, and muscle strips from these bladders were more sensitive than those from sham-operated controls to a cholinergic agonist. In vitro bFGF treatment increased connexin 43 expression in cultured rat BSMC via the ERK 1/2 pathway. This finding was supported by another in vivo model, where bFGF released from gelatin hydrogels fixed on rat bladder walls caused connexin 43 upregulation and gap junction formation in the muscle layer. Bladder muscle strips in this model showed increased sensitivity to a cholinergic agonist that was blocked by inhibition of gap junction function with α-glycyrrhetinic acid. Cystometric analyses of this model showed typical features of detrusor overactivity such as significantly increased micturition frequency and decreased bladder capacity. These findings suggest that bFGF from the urothelium could induce bladder hypersensitivity to acetylcholine via gap junction generation in the smooth muscle, thereby contributing to the myogenic overactivity of obstructed bladders.

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mentioning

confidence: 65%

Basic fibroblast growth factor causes urinary bladder overactivity through gap junction generation in the smooth muscle

Imamura¹,

Negoro²,

Kanematsu³

et al. 2009

American Journal of Physiology-Renal Physiology

View full text Add to dashboard Cite

show abstract

“…Gap junctions are important for normal coupling in contractile organs. Several authors reported changes in expression of connexins (gap junction proteins) in various models of bladder overactivity [Hae£iger et al, 2002;Christ et al, 2003;Mori et al, 2005]. More research is required to elucidate the functional signi¢cance of these observations.…”

Section: Intrinsic Propertiesmentioning

confidence: 99%

Comparison study of autonomous activity in bladders from normal and paraplegic rats

Gevaert

Ost

Ridder

2006

Neurourology and Urodynamics

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“…Christ et al (7) showed a 75-fold increase of Cx43 mRNA expression compared with the control in DO cells in rats after 6 wk of PBOO, whereas others using scrape loading dye transfer (SLDT) found an increase in dye transfer in the bladder urothelial cells of the rats with acute bladder outflow obstruction. Mori et al (21) revealed an initial increase in Cx43 mRNA expression, but this was followed by a secondary decrease. The inconsistencies might be due to variations in the time course of the PBOO or the animal model used.…”

mentioning

confidence: 96%

Changes of gap junctional cell-cell communication in overactive detrusor in rats

Li¹,

Jiang²,

Hao³

et al. 2007

American Journal of Physiology-Cell Physiology

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To evaluate the changes in intercellular communication through gap junctions in detrusor overactivity (DO), we studied 23 adult female Wistar rats with DO after partial outflow obstruction (DO group) and 13 sham-operated rats (control group). The two groups were compared by means of urodynamics, light and electron microscopy, expression of Cx40, Cx43, and Cx45 mRNA genes with RT-PCR, Cx43 protein with Western blot analysis, and functional intercellular communication with scrape loading dye transfer (SLDT) and fluorescence recovery after photobleaching (FRAP). The number of gap junctions and the expression of connexin mRNA and Cx43 protein were increased in DO rats, and intercellular communication through gap junctions increased after 6 wk of partial outflow obstruction as assessed with SLDT and FRAP techniques. The findings provide a theoretical rationale for using Cx43 antagonists and gap junction inhibitors in the treatment of patients with overactive detrusor secondary to partial bladder outflow obstruction.

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Decreased cellular membrane expression of gap junctional protein, connexin 43, in rat detrusor muscle with chronic partial bladder outlet obstruction

Cited by 22 publications

References 20 publications

Basic fibroblast growth factor causes urinary bladder overactivity through gap junction generation in the smooth muscle

Basic fibroblast growth factor causes urinary bladder overactivity through gap junction generation in the smooth muscle

Comparison study of autonomous activity in bladders from normal and paraplegic rats

Changes of gap junctional cell-cell communication in overactive detrusor in rats

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