Basic fibroblast growth factor modulates proliferation and collagen expression in urinary bladder smooth muscle cells

Imamura, Masaaki; Kanematsu, Akihiro; Yamamoto, Shingo; Kimura, Yu; Kanatani, Isao; Ito, Noriyuki; Tabata, Yasuhiko; Ogawa, Osamu

doi:10.1152/ajprenal.00107.2007

Cited by 54 publications

(66 citation statements)

References 57 publications

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“…BSMC were isolated from 9-wk-old female SpragueDawley rats (Japan Slc, Shizuoka, Japan) using a procedure described previously (14,19). Cells after two passages were seeded at 2 ϫ 10 4 cells/ml in six-well plates for Western blot analysis or on chamber slides for immunofluorescence, and then serum-deprived in DMEM containing 0.5% FCS for 48 h before each assay.…”

Section: Methodsmentioning

confidence: 99%

“…One is the mechanism of connexin 43 upregulation and the other is the functional involvement of connexin 43 in detrusor hypersensitivity. Regarding the former issue, our previous study demonstrated a regulatory effect of basic fibroblast growth factor (bFGF) on BSMC remodeling in the obstructed bladder with specific alterations of collagen production and BSMC proliferation (14). Since bFGF has been reported to stimulate connexin 43 expression in cardiac myocytes and fibroblasts (7,8), we postulated that the same mechanism that regulates collagen production and cell proliferation could also regulate connexin 43 expression in the obstructed bladder.…”

mentioning

confidence: 99%

“…Next, the regulatory role of bFGF on connexin 43 expression in BSMC was investigated using an in vitro BSMC culture system. Finally, the physiological effects of bFGF on bladder smooth muscle were explored in our original in vivo animal model, where a gelatin hydrogel incorporating bFGF was employed as a carrier for sustained release (14,15,32,35,36).…”

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confidence: 99%

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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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Section: Methodsmentioning

confidence: 99%

mentioning

confidence: 99%

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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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“…At the same time, the elasticity of the nonshrunken graft should be preserved; this is directly related to development of well-developed and organized smooth muscle bundles derived from the edges of the bladder that traverse the graft, organize and then develop into mature muscles [18].…”

Section: Discussionmentioning

confidence: 99%

Full-Thickness Hysterocystoplasty for Management of a Large Bladder Defect: Experimental Study in Goats

Abdelrhman

Seddek

Bakr

et al. 2013

The Journal of Veterinary Medical Science

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ABSTRAcT. The uterine tissue of three healthy nonpregnant goats was evaluated experimentally as a graft for closure of a bladder defect. Goats were subjected to ovariectomy, and then one detubularized uterine horn was used as a graft to close a large defect in the ventral aspect of the bladder. Follow up included monthly radiographic and ultrasonographic examinations and evaluations of kidney function and electrolytes changes for six months. The goats were euthanized after six months, and both the bladder and the graft were examined macroscopically and histologically. The technique required less invasive procedures than those described with alternative techniques of cystoplasty, achieved a high survival rate without life-threatening complications post surgery, was associated with no significant changes in kidney function and electrolytes levels, showed proper healing of the transplanted graft by regeneration rather than repair without scaring or fibrosis and with complete covering of the graft by a healthy urothelium and was associated with no malignant transformation. Hysterocystoplasty is a noninvasive, non-life-threatening technique due to the close position of the bladder to the uterus, and proper healing of the graft reflects absence of pressure on its blood supply. It is an acceptable alternative technique for closure of a large bladder defect and avoids disadvantages of alternative techniques of cystoplasty. It might be accepted by owners of pets, and further studies in clinical cases of dogs are advised. Although cystoplasty is a historic topic that has been discussed well in scientific literature and argued at legendary proportion among urologists, the search for an ideal organ to replace a diseased bladder remains elusive for reconstructive urologists [32]. Many augmentation cystoplasty or neobladder techniques have been used routinely for treatment of reduced bladder compliance and capacity secondary to bladder infection and inflammation [27], neurogenic dysfunction or congenital bladder disorders [16], detrusor over activity [10], large bladder defects [8,9], bladder necrosis [30] and bladder tumors [7,12]. Although encouraging animal and human results have been reported with different techniques, each technique had its own limitations, complications and disadvantages [2,4,11,27].The ileum and colon have been used for decades for reconstruction of the bladder, in spite of the harmful contact of urine with the mucosa of the augmenting patch [23], which is predisposed to multiple short-and/or long-term complications like chronic bacteriuria or mucous secretion [1,23], stone formation [1,11,29], disturbance of calciumphosphate metabolism with potential bone growth retardation [24,28], altered hepatic and electrolyte metabolism [24], gastrointestinal motility disorders [23], augmenting patch perforation [1,6] and malignant transformation of the augmenting patch [1,14].Gastrocystoplasty has been described as an alternative technique; unfortunately, as the popularity of gastrocystoplasty increased, so did ...

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“…The opposite face of the scaffold could them be modified using a second component, which in this case was a mixture of PGA and urothelial cells, since these cells could potentially send necessary signals to smooth muscle cells during regeneration. (Beqaj, 2005;Imamura, 2007) When the human bladder smooth muscle cells and urothelial cells where embedded in a PA-scaffold with a growth factor (bFGF) and incubated in vivo in a subcutaneous nude rat model, it was found that the human bladder smooth muscle cells were retained and composed the majority of the scaffold cellular content. It was also found that the system which uses a combination of PGA, PA, growth factors and cells demonstrated higher levels of phenotypic alpha-smooth muscle actin than control scaffolds made of PGA and cells only.…”

Section: Bioactive Peptides and Peptide Amphiphiles For Regeneration mentioning

confidence: 99%

Aspects of Urological Tissue Engineering

Sharma¹,

Rożkiewicz²

2011

Tissue Engineering for Tissue and Organ Regeneration

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Basic fibroblast growth factor modulates proliferation and collagen expression in urinary bladder smooth muscle cells

Cited by 54 publications

References 57 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

Full-Thickness Hysterocystoplasty for Management of a Large Bladder Defect: Experimental Study in Goats

Aspects of Urological Tissue Engineering

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