Structural alterations of the bladder induced by detrusor instability: experimental study in rabbits

Amaro, João Luiz; Balasteghin, Karina Tuma; Padovani, Carlos Roberto; Montenegro, Renata de Lello

doi:10.1590/s1677-55382005000600012

Cited by 8 publications

(10 citation statements)

References 28 publications

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“…Similar results were also reported in several previous studies (de Boer et al. 1994; Amaro et al. 2005; Bouchelouche et al.…”

Section: Discussionsupporting

confidence: 93%

“…The IVO14 groups continued to demonstrate inflammatory infiltration, but the cell types were different, consisting mainly of macrophage. Similar results were also reported in several previous studies (de Boer et al 1994;Amaro et al 2005;Bouchelouche et al 2006;Anumanthan et al 2009). What caught our attention in this study is that amitriptyline did not affect the inflammatory infiltration process, which was interesting because studies have shown that tricyclic antidepressants (TCAs) inhibit the release of inflammatory mediators, such as IL-6, IL-1b and TNF-a (Xia et al 1996;Yaron et al 1999;Tai et al 2009).…”

Section: Discussionsupporting

confidence: 92%

“…Observation of hypertrophy of the detrusor tunic was expected, reflecting the compensatory response observed early in chronic bladder outlet obstruction (Zhang et al. 2004; Amaro et al. 2005; Lepor 2005; Fujita et al.…”

Section: Discussionmentioning

confidence: 91%

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Amitriptyline aggravates the fibrosis process in a rat model of infravesical obstruction

Prado

Soares

Lima

et al. 2012

Int J Experimental Path

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Infravesical obstruction (IVO) secondary to benign prostatic hypertrophy can affect up to 50% of men over 50 years old and may cause serious and irreversible alterations throughout the urinary tract, especially in the bladder. Therapeutic approaches are currently limited. Amitriptyline has recently been described as an analgesic, anti-inflammatory and myorelaxant in some experimental models. The objective of this study was to investigate the effects of amitriptyline hydrochloride on the process of fibrosis in a bladder outlet obstruction model in rats. Male Wistar rats were subjected to IVO and studied at intervals of 1 and 14 days postprocedure. The rats were randomly divided into five groups: sham, IVO1-T, IVO1-NT, IVO14-T and IVO14-NT. Bladder tissue was processed for histopathology, immunohistochemistry and RT-PCR. The IVO14 groups presented bladder fibrosis, smooth muscle cell hypertrophy and bladder wall thickening. The IVO14-T group demonstrated a higher intensity of fibrosis, higher macrophage infiltration rate and higher gene expression of Transforming growth factor (TGF) Tgf-β1. Thus this data shows that in this experimental mode amitriptyline had an amplifying effect on the process of fibrosis as a whole.

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“…Similar results were also reported in several previous studies (de Boer et al. 1994; Amaro et al. 2005; Bouchelouche et al.…”

Section: Discussionsupporting

confidence: 93%

Section: Discussionsupporting

confidence: 92%

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Amitriptyline aggravates the fibrosis process in a rat model of infravesical obstruction

Prado

Soares

Lima

et al. 2012

Int J Experimental Path

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“…Rat wild-type (pRK7-HA-S6K1-WT) and constitutively active S6K clones (pRK7-HA-S6K1-E389, -E389D3E) 7 were obtained from Addgene. Primary BSMC were transfected using LTX and Plus reagent as recommended by the manufacturer (Invitrogen, Carlsbad, CA).…”

Section: Transfections With Myc-mtor and Ha-s6kmentioning

confidence: 99%

Mammalian Target of Rapamycin (mTOR) Induces Proliferation and De-Differentiation Responses to Three Coordinate Pathophysiologic Stimuli (Mechanical Strain, Hypoxia, and Extracellular Matrix Remodeling) in Rat Bladder Smooth Muscle

Aitken

Tölg

Panchal

et al. 2010

The American Journal of Pathology

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Maladaptive bladder muscle overgrowth and de-differentiation in human bladder obstructive conditions is instigated by coordinate responses to three stimuli: mechanical strain , tissue hypoxia , and extracellular matrix remodeling.1 ,2 Pathway analysis of genes induced by obstructive models of injury in bladder smooth muscle cells (BSMCs) identified a mammalian target of rapamycin (mTOR)-specific inhibitor as a potential pharmacological inhibitor. Strain-induced mTOR-specific S6K activation segregated differently from ERK1/2 activation in intact bladder ex vivo. Though rapamycin's antiproliferative effects in vascular smooth muscle cells are well known , its effects on BSMCs were previously unknown. Rapamycin significantly inhibited proliferation of BSMCs in response to mechanical strain , hypoxia , and denatured collagen. Rapamycin inhibited S6K at mTOR-sensitive phosphorylation sites in response to strain and hypoxia. Rapamycin also supported smooth muscle actin expression in response to strain or hypoxia-induced de-differentiation. Importantly , strain plus hypoxia synergistically augmented mTOR-dependent S6K activation , Mmp7 expression and proliferation. Forced expression of wild-type and constitutively active S6K resulted in loss of smooth muscle actin expression. Decreased smooth muscle actin , increased Mmp7 levels and mTOR pathway activation during in vivo partial bladder obstruction paralleled our in vitro studies. These results point to a coordinate role for mTOR in BSMCs responses to the three stimuli and a potential new therapeutic target for myopathic bladder disease.

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“…The most widely used animal is the rabbit, but the pig, rat, and mouse also have been used [7–11]. Although there are significant differences among animal models of PBOO, there are many similarities among these models and the obstructive dysfunction seen in humans.…”

Section: Introductionmentioning

confidence: 99%

Bladder outlet obstruction in male cystinuria mice

Ercolani¹,

Sahota

Schuler

et al. 2009

Int Urol Nephrol

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Background Cystinuria is the most common inherited cause of urinary tract stones in children. It can lead to obstructive uropathy, which is a major cause of renal failure. Genetic studies have identified two genes, SLC3A1 and SLC7A9, to be directly involved in cystine stone formation. Slc3a1 knockout male mice develop cystine stones in the bladder and, to a lesser extent, in the kidney. Slc3a1 knockout female mice also develop cystinuria, but they do not form stones. The specific aim of this study was to characterize bladder function in cystinuria mice. Methods Eight control (4 male, 4 female) and 16 Slc3a1 knockout (9 male, 7 female) mice of mixed strain background (C57B/129, age 4–5 months) were evaluated. Each mouse was anesthetized and the bladder dome catheterized for cystometry. Immediately following cystometry, the bladder was excised, weighed, and separated into three full thickness strips for contractile studies. Results Bladders from cystinuria male mice had significantly increased weight, all of them had stones, decreased compliance, and decreased contractile responses to field stimulation, ATP, carbachol, and KCl. Compared with controls, female knockout mice showed normal bladder weight, decreased voiding pressure, slightly decreased compliance, and slightly decreased contractile responses. Conclusions These studies clearly demonstrate that the bladder stones that developed in the male cystinuria mice resulted in a partial outlet obstruction. Although the female cystinuria mice did not have bladder stones, bladder function was mildly impaired; presumably by the presence of cystine crystals.

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Structural alterations of the bladder induced by detrusor instability: experimental study in rabbits

Abstract: Detrusor instability induced by partial bladder outlet obstruction caused significant histopathological and immunohistochemical alterations in the bladder of rabbits.

Cited by 8 publications

References 28 publications

Amitriptyline aggravates the fibrosis process in a rat model of infravesical obstruction

Amitriptyline aggravates the fibrosis process in a rat model of infravesical obstruction

Mammalian Target of Rapamycin (mTOR) Induces Proliferation and De-Differentiation Responses to Three Coordinate Pathophysiologic Stimuli (Mechanical Strain, Hypoxia, and Extracellular Matrix Remodeling) in Rat Bladder Smooth Muscle

Bladder outlet obstruction in male cystinuria mice

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