Enhanced expression of mast cell growth factor and mast cell activation in the bladder following the resolution of trinitrobenzenesulfonic acid (TNBS) colitis in female rats

Liang, Ruomei; Ustinova, Elena E.; Patnam, Radhika; Fraser, Matthew O.; Gutkin, Dmitriy W.; Pezzone, Michael A.

doi:10.1002/nau.20410

Cited by 21 publications

(22 citation statements)

References 58 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Similar phenomenon has also been seen in the urinary bladder of animals with colitis. After 2,4,6-Trinitrobenzenesulfonic acid treatment, the urinary bladder becomes overactive which is accompanied by an increase in the mast cell numbers with no change in the activity of Akt [44–46]. …”

Section: Discussionmentioning

confidence: 99%

The urinary bladder of spontaneously hypertensive rat demonstrates bladder hypertrophy, inflammation, and fibrosis but not hyperplasia

2015

View full text Add to dashboard Cite

The present study aims to systemically characterize the factors that are associated with urinary bladder organ enlargement in the spontaneously hypertensive rats (SHR). Material and Methods We compared the SHR to age-matched normotensive Wistar-Kyoto (WKY) control rats in the levels of bladder pro-inflammatory factors, collagen expression (type I), and detrusor smooth muscle growth. Key Findings Our results showed that enhanced inflammatory responses and fibrosis were key factors that were closely associated with bladder wall thickening in SHR. Specifically the mRNA levels of inflammatory factors interleukin (IL)-1α, IL-6 and TNFα were significantly higher in SHR than those in WKY. The SHR also had a higher number of mast cells in the suburothelium space. Type I collagen production was also significantly higher in SHR when compared to those in control rats. However, the smooth muscle content stayed the same in SHR and WKY rats. This was shown as that the ratio of α-smooth muscle actin (SMA) to the nuclear protein histone H3 showed no difference between these two rat strains. The mRNA and protein levels of proliferating cell nuclear antigen (PCNA) also showed no change in the urinary bladder of SHR and WKY. Further study showed that the phosphorylation level of Akt in the urinary bladder was not changed in SHR when compared to WKY. In contrast, the phosphorylation level of ERK1/2 was significantly higher in SHR bladder when compared to WKY. Significance These results suggest that inflammation and fibrosis are primary factors that may lead to urinary bladder hypertrophy in SHR.

show abstract

Section: Discussionmentioning

confidence: 99%

The urinary bladder of spontaneously hypertensive rat demonstrates bladder hypertrophy, inflammation, and fibrosis but not hyperplasia

2015

View full text Add to dashboard Cite

show abstract

“…Several examples of cross-organ sensitization have been demonstrated in the pelvic viscera, including chemically induced colitis in rats that induced urinary frequency, bladder afferent fiber hyperexcitability (35,51), upregulation of the NGF mRNA levels and mast cell infiltration in the bladder (22,52), and increased excitability of bladder afferent neurons, as well as spinal dorsal horn neurons receiving inputs from the bladder (25,37). The NGF levels are reportedly elevated in the bladders of patients with benign prostatic hyperplasia (46), idiopathic OAB, and interstitial cystitis (23).…”

Section: Discussionmentioning

confidence: 99%

Association of overactive bladder and stress urinary incontinence in rats with pudendal nerve ligation injury

Furuta

Kita²,

Suzuki³

et al. 2008

American Journal of Physiology-Regulatory, Integrative and Comp

View full text Add to dashboard Cite

Approximately one-third of patients with stress urinary incontinence (SUI) also suffer from urgency incontinence, which is one of the major symptoms of overactive bladder (OAB) syndrome. Pudendal nerve injury has been recognized as a possible cause for both SUI and OAB. Therefore, we investigated the effects of pudendal nerve ligation (PNL) on bladder function and urinary continence in female Sprague-Dawley rats. Conscious cystometry with or without capsaicin pretreatment (125 mg/kg sc), leak point pressures (LPPs), contractile responses of bladder muscle strips to carbachol or phenylephrine, and levels of nerve growth factor (NGF) protein and mRNA in the bladder were compared in sham and PNL rats 4 wk after the injury. Urinary frequency detected by a reduction in intercontraction intervals and voided volume was observed in PNL rats compared with sham rats, but it was not seen in PNL rats with capsaicin pretreatment that desensitizes C-fiber-afferent pathways. LPPs in PNL rats were significantly decreased compared with sham rats. The contractile responses of detrusor muscle strips to phenylephrine, but not to carbachol, were significantly increased in PNL rats. The levels of NGF protein and mRNA in the bladder of PNL rats were significantly increased compared with sham rats. These results suggest that pudendal nerve neuropathy induced by PNL may be one of the potential risk factors for OAB, as well as SUI. Somato-visceral cross sensitization between somatic (pudendal) and visceral (bladder) sensory pathways that increases NGF expression and alpha(1)-adrenoceptor-mediated contractility in the bladder may be involved in this pathophysiological mechanism.

show abstract

“…While the exact mechanism is not known, the role of PNAs in the development of visceral sensitivity has recently received much attention. In adult rats, colon irritation with TNBS sensitizes bladder PNAs to mechanical and chemical irritation and has also been shown to increase the percentage of activated masts cells in the bladder (18,19). In adult rats, acute bladder inflammation with KCL has been shown to produces cross-sensitization of pelvic afferents and colon hypersensitivity to mechanical distension (20).…”

Section: Introductionmentioning

confidence: 99%

Neonatal cystitis-induced colonic hypersensitivity in adult rats: a model of viscero-visceral convergence

Miranda

Mickle

Schmidt

et al. 2011

Neurogastroenterology &Amp; Motility

View full text Add to dashboard Cite

Background The objective of this study was to determine if neonatal cystitis alters colonic sensitivity later in life and to investigate the role of peripheral mechanisms. Methods Neonatal rats received intravesical zymosan, normal saline, or anesthesia only for three consecutive days (postnatal days 14th–16th). The estrous cycle phase was determined prior to recording the visceromotor response (VMR) to colorectal distension (CRD) in adult rats. Eosinophils and mast cells were examined from colon and bladder tissue. CRD or urinary bladder distension (UBD)-sensitive pelvic nerve afferents (PNAs) were identified and their responses to distension were examined. The relative expression of N-methyl-D-aspartic acid (NMDA) NR1 subunit in the L6-S1 spinal cord was examined using Western blot. Results The VMR to CRD (≥10mmHg) in the neonatal zymosan group was significantly higher than control in both the diestrus, estrus phase and in all phases combined. There was no difference in the total number of eosinophils, mast cells or number of degranulated mast cells between groups. The spontaneous firing of UBD, but not CRD-sensitive PNAs from the zymosan rats was significantly higher than the control. However, the mechanosensitive properties of PNAs to CRD or UBD were no different between groups (p > 0.05). The expression of spinal NR1 subunit was significantly higher in zymosan-treated rats compared to saline treated rats (p <0.05). Conclusion Neonatal cystitis results in colonic hypersensitivity in adult rats without changing tissue histology or the mechanosensitive properties of CRD-sensitive PNAs. Neonatal cystitis does results in overexpression of spinal NR1 subunit in adult rats.

show abstract

Enhanced expression of mast cell growth factor and mast cell activation in the bladder following the resolution of trinitrobenzenesulfonic acid (TNBS) colitis in female rats

Cited by 21 publications

References 58 publications

The urinary bladder of spontaneously hypertensive rat demonstrates bladder hypertrophy, inflammation, and fibrosis but not hyperplasia

The urinary bladder of spontaneously hypertensive rat demonstrates bladder hypertrophy, inflammation, and fibrosis but not hyperplasia

Association of overactive bladder and stress urinary incontinence in rats with pudendal nerve ligation injury

Neonatal cystitis-induced colonic hypersensitivity in adult rats: a model of viscero-visceral convergence

Contact Info

Product

Resources

About