Mini-pig urinary bladder function: comparisons of in vitro anticholinergic responses and in vivo cystometry with drugs indicated for urinary incontinence

Introduction and hypothesis: Pelvic support structure injury is the major cause of pelvic organ prolapse. At present, polypropylene-based filler material has been suggested as a common method to treat pelvic organ prolapse. However, it cannot functionally rehabilitate the pelvic support structure. In addition to its poor long-term efficiency, the urinary bladder matrix was the most suitable biological scaffold material for pelvic floor repair. Here, we hypothesize that anti-sca-1 monoclonal antibody and basic fibroblast growth factor were cross-linked to urinary bladder matrix to construct a two-factor bioscaffold for pelvic reconstruction. Methods Through a bispecific cross-linking reagent, sulfosuccinimidyl 4-[N-maleimidomethyl] cyclohexane-1-carboxylate (sulfo-smcc) immobilized anti-sca-1 and basic fibroblast growth factor to urinary bladder matrix. Then scanning electron microscope and plate reader were used to detect whether the anti-sca-1/basic fibroblast growth factor-urinary bladder matrix scaffold was built successfully. After that, the capacity of enriching sca-1 positive cells was measured both in vitro and in vivo. In addition, we evaluated the differentiation capacity and biocompatibility of the scaffold. Finally, western blotting was used to detect the level of fibulin-5 protein. Results The scanning electron microscope and plate reader revealed that the double-factor biological scaffold was built successfully. The scaffold could significantly enrich a large number of sca-1 positive cells both in vitro and in vivo, and obviously accelerate cells and differentiate functional tissue with good biocompatibility. Moreover, the western blotting showed that the scaffold could improve the expression of fibulin-5 protein. Conclusion The anti-sca-1/basic fibroblast growth factor-urinary bladder matrix scaffold revealed good biological properties and might serve as an ideal scaffold for pelvic reconstruction.

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MiADMSA ameliorate arsenic induced urinary bladder carcinogenesis in vivo and in vitro

Biomedicine & Pharmacotherapy ◽

10.1016/j.biopha.2020.110257 ◽

2020 ◽

Vol 128 ◽

pp. 110257 ◽

Cited By ~ 2

Author(s):

Kshirod Sathua ◽

Sakshi Srivastava ◽

S.J.S. Flora

Keyword(s):

Urinary Bladder ◽

Bladder Carcinogenesis

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A reinvestigation of the function of the mammalian urinary bladder

AJP Renal Physiology ◽

10.1152/ajprenal.1977.232.3.f187 ◽

1977 ◽

Vol 232 (3) ◽

pp. F187-F195 ◽

Cited By ~ 1

Author(s):

S. A. Lewis

Keyword(s):

Urinary Bladder ◽

Membrane Surface ◽

Apical Cell ◽

Membrane Damage ◽

In Vitro Experiments ◽

Apical Cell Membrane ◽

Cell Membrane Damage ◽

Using Data

The function of adult mammalian urinary bladder is evaluated in light of recent in vitro experiments. The discrepancy between in vivo and in vitro experimental results is examined and a possible solution proposed. Techniques for eliminating edge damage and measuring apical membrane surface area are described. A new chamber design for microelectrode studies is illustrated. The possibility of apical cell membrane damage caused by microelectrodes is critically examined and tested using the polyene antibiotic Nystatin. Using data from transepithelial and microelectrode experiments, a model for net Na+ transport across the bladder is proposed and then critically analyzed. The possible clinical implications of the in vitro experiments are briefly discussed.

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Regenerative potential of human dental pulp stem cells in the treatment of stress urinary incontinence: In vitro and in vivo study

Cell Proliferation ◽

10.1111/cpr.12675 ◽

2019 ◽

Vol 52 (6) ◽

Cited By ~ 4

Author(s):

Alessio Zordani ◽

Alessandra Pisciotta ◽

Laura Bertoni ◽

Giulia Bertani ◽

Antonio Vallarola ◽

...

Keyword(s):

Stem Cells ◽

Urinary Incontinence ◽

Stress Urinary Incontinence ◽

Dental Pulp ◽

Dental Pulp Stem Cells ◽

In Vivo Study ◽

Human Dental Pulp

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Protective Effects of Antimuscarinics on the Bladder Remodeling After Bladder Outlet Obstruction

Cellular Physiology and Biochemistry ◽

10.1159/000485358 ◽

2017 ◽

Vol 44 (3) ◽

pp. 907-919 ◽

Cited By ~ 7

Author(s):

Qiang Liu ◽

Deyi Luo ◽

Tongxin Yang ◽

Banghua Liao ◽

Hong Li ◽

...

Keyword(s):

Smooth Muscle ◽

Bladder Outlet Obstruction ◽

Outlet Obstruction ◽

Structure And Function ◽

Bladder Function ◽

Bladder Smooth Muscle ◽

M3 Receptors ◽

And Function

Background/Aims: Overactive bladder associated with bladder outlet obstruction (BOO) is a highly prevalent condition, which is usually treated with antimuscarinics. However, the potential effects of antimuscarinics on the structure and function of bladder have not been investigated thus far. Methods: Sprague-Dawley(R) rats accepted bladder neck obstruction surgery or sham surgery, and then received treatment of three different antimuscarinics (Solifenacin, Darifenacin, and Tolterodine) or vehicle. After 3, 6 and 12 weeks, the bladder function and structure were measured. The effect of antimuscarinics on cellular alteration in vitro was observed under mechanical stimulation. Bladder morphology were examined by immunohistochemistry, and the bladder function were investigated by cystometry and strip contractility test. The expression of muscarinic receptors and inflammatory cytokines were measured by PCR and Western blotting. Results: Here we demonstrate, both in vitro and in vivo, that antimuscarinics are protective regulators for the bladder structure and function. Antimuscarinics decrease the weight of bladders with BOO. Antimuscarinics improve the voiding parameter and enhance the contraction of bladder smooth muscle. The results also show that antimuscarinics inhibit the proliferation of bladder smooth muscle cells both in vivo and in vitro, it can reduce the collagen deposition and inflammatory cytokines in bladders with BOO. During this process, the expression of M2 and M3 receptors was altered by antimuscarinics. Conclusion: Antimuscarinics could reverse the structural and functional changes of BOO bladder wall at cellular and tissue level, and the alteration of M2 and M3 receptors may be involved in this biological process.

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