Preservation of uroplakins by 2-mercaptoethanesulfonate in cyclophosphamide-induced rat cystitis

Kyung, Yoon Soo; Park, Hee Yoon; Lee, Gil‐Ho

doi:10.1007/s00204-010-0523-y

Cited by 17 publications

(59 citation statements)

References 18 publications

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“…[29][30][31] Mucosal lesions, such as edema or hemorrhage, will occur and mucosal permeability will increase after CYP treatment. 32 It is suspected that nitric oxide release, 33 inflammation and hyperactivity 34 after CYP treatment is associated with the disruption of mucosa.…”

Section: Discussionmentioning

confidence: 99%

Effect of hyaluronic acid on urine nerve growth factor in cyclophosphamide‐induced cystitis

Cheng

Lin

et al. 2011

Int J of Urology

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Objectives: To investigate how hyaluronic acid (HA) affects nerve growth factor (NGF) production and bladder overactivity in a cyclophosphamide (CYP)-induced cystitis rat model. Methods: Female Sprague-Dawley rats received three intermittent intraperitoneal injections of CYP (75 mg/kg) or saline. Before or after CYP injection, HA was given intravesically and urine NGF was checked with creatinine correction. Bladder function was evaluated by cystometrograms under Zoletil anesthesia. Furthermore, the effect of HA was counteracted with hyaluronidase (HYAL). Bladder structural change was compared among groups with trichrome stain. Results: The intercontraction interval (ICI) significantly decreased in CYP-injected rats in comparison to the salineinjected controls. In the CYP-injected groups, bladder HA instillation significantly increased the ICI, but did not change the maximum voiding pressure in comparison to the saline instillation. NGF production significantly increased in CYP-injected rats, but decreased significantly with HA treatment. Treatment with HA had a more significant effect on urine NGF and the use of HYAL would eliminate this effect. Specific staining showed mucosa swelling after CYP treatment. Little HA coating on bladder mucosa could be found in HA-treated rats. Conclusions: Present findings raise the possibility that HA could be an effective treatment for CYP-related bladder overactivity through the involvement of NGF signaling.

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Section: Discussionmentioning

confidence: 99%

Effect of hyaluronic acid on urine nerve growth factor in cyclophosphamide‐induced cystitis

Cheng

Lin

et al. 2011

Int J of Urology

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“…After rats received an intramuscular injection of ketamine (15 mg/kg) and xylazine (5 mg/kg) for anesthesia, they received an intraperitoneal injection of 150 mg CYP/kg (SigmaAldrich St. Louis, MO, USA) dissolved in 1 mL of distilled water (Kyung et al 2011). A polyethylene catheter (PE-10) was inserted into the urethra of each rat to evacuate the urine in the bladder.…”

Section: Animalsmentioning

confidence: 99%

“…PCR primer sequences for UPII were reported (Kyung et al 2011). The ImProm-II TM Reverse Transcription System (Promega, Madison, WI, USA) was used to prepare cDNA according to the manufacturer's instructions.…”

Section: Gene Expression Of Upii As Determined By Rt-pcrmentioning

confidence: 99%

“…Recently, we developed a quantitative real-time polymerase chain reaction (RT-PCR) assay to measure the levels of uroplakins (UPs), which constitute the most impermeable barriers in the body, from rat urinary bladder (Kyung et al 2011). Uroplakin II (UPII) expression among four UP subunits (UPIa, UPIb, UPII, and UPIII) in urinary bladder strongly correlates with the histopathological parameters for hemorrhage cystitis in CYP-induced animal models of cystitis (Kyung et al 2011).…”

Section: Introductionmentioning

confidence: 99%

“…Uroplakin II (UPII) expression among four UP subunits (UPIa, UPIb, UPII, and UPIII) in urinary bladder strongly correlates with the histopathological parameters for hemorrhage cystitis in CYP-induced animal models of cystitis (Kyung et al 2011). Epinephrine (EPI) is a promising drug to decrease the incidence and severity of CYP-induced rat cystitis (Chow et al 2006).…”

Section: Introductionmentioning

confidence: 99%

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Intravesical epinephrine preserves uroplakin II expression in urinary bladder from cyclophosphamide-induced rat cystitis

Kyung

Park

Lee

2012

Naunyn-Schmiedeberg's Arch Pharmacol

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We investigated the attenuated effect of intravesical epinephrine (EPI) on uroplakin II (UPII) expression in cyclophosphamide (CYP)-induced rat cystitis. Sixty-eight Sprague-Dawley female rats were divided into one negative control group (GI) and five intraperitoneally CYP (150 mg CYP/kg)-injected groups (GII-VI) consisting of a positive control group (GII), three groups (GIII-V) with retaining intravesically instillated ameliorating agents for 90 min by urethral ligation until sacrifice, and one group (GVI) with freely voiding after intravesical EPI instillation. The retention groups were further classified into null-treated- (GIII), EPI- (GIV), and vehicle group (GV). All rats were euthanized 24 h after CYP injection. The UPII and α1-adrenergic receptors (AR) levels were measured with real-time polymerase chain reaction (RT-PCR) method and the morphological changes were also evaluated. CYP induced severe cystitis and decreased vesical UPII mRNA level. The EPI-treated groups had showed attenuation effects against submucosal edema and hemorrhage, and preserved UPII expression. Concurrently, intravesical EPI resulted in a significant preservation of both subtypes of α1A- and α1B AR expressions, which was well correlated with the hemostatic pattern in the samples. The obstructed and null-treated group (GIII) revealed severe cystitis and maximally decreased UPII levels, and the diluting effect of vehicle (GV) on CYP toxicity was insignificant on UPII preservation. The UPII level of RT-PCR was well correlated with the UPII immunohistological expression and their morphological changes. Intravesical instillation of EPI preserves UPII expression and attenuates the toxic responses in the bladder in CYP-induced rat cystitis.

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Therapeutic exploitation of IPSE, a urogenital parasite‐derived host modulatory protein, for chemotherapy‐induced hemorrhagic cystitis

Mbanefo

Pennington

et al. 2018

FASEB j.

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Chemotherapy-induced hemorrhagic cystitis (CHC) can be difficult to manage. Prior work suggests that IL-4 alleviates ifosfamide-induced hemorrhagic cystitis (IHC), but systemically administered IL-4 causes significant side effects. We hypothesized that the Schistosoma hematobium homolog of IL-4-inducing principle from Schistosoma mansoni eggs (H-IPSE), would reduce IHC and associated bladder pathology. IPSE binds IgE on basophils and mast cells, triggering IL-4 secretion by these cells. IPSE is also an “infiltrin,” translocating into the host nucleus to modulate gene transcription. Mice were administered IL-4, H-IPSE protein or its nuclear localization sequence (NLS) mutant, with or without neutralizing anti-IL-4 antibody, or 2-mercaptoethane sulfonate sodium (MESNA; a drug used to prevent IHC), followed by ifosfamide. Bladder tissue damage and hemoglobin content were measured. Spontaneous and evoked pain, urinary frequency, and bladdergene expression analysis were assessed. Pain behaviors were interpreted in a blinded fashion. One dose of H-IPSE was superior to MESNA and IL-4 in suppressing bladder hemorrhage in an IL-4-dependent fashion and comparable with MESNA in dampening ifosfamide-triggered pain behaviors in an NLS-dependent manner. H-IPSE also accelerated urothelial repair following IHC. Our work represents the first therapeutic exploitation of a uropathogen-derived host modulatory molecule in a clinically relevant bladder disease model and indicates that IPSE may be an alternative to MESNA for mitigating CHC.—Mbanefo, E. C., Le, L., Pennington, L. F., Odegaard, J. I., Jardetzky, T. S., Alouffi, A., Falcone, F. H., Hsieh, M. H. Therapeutic exploitation of IPSE, a urogenital parasite-derived host modulatory protein, for chemotherapy-induced hemorrhagic cystitis.

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Preservation of uroplakins by 2-mercaptoethanesulfonate in cyclophosphamide-induced rat cystitis

Cited by 17 publications

References 18 publications

Effect of hyaluronic acid on urine nerve growth factor in cyclophosphamide‐induced cystitis

Effect of hyaluronic acid on urine nerve growth factor in cyclophosphamide‐induced cystitis

Intravesical epinephrine preserves uroplakin II expression in urinary bladder from cyclophosphamide-induced rat cystitis

Therapeutic exploitation of IPSE, a urogenital parasite‐derived host modulatory protein, for chemotherapy‐induced hemorrhagic cystitis

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