Impaired Expression of Prostaglandin E2 (PGE2) Synthesis and Degradation Enzymes during Differentiation of Immortalized Urothelial Cells from Patients with Interstitial Cystitis/Painful Bladder Syndrome

Marentette, John; Hurst, Robert E.; McHowat, Jane

doi:10.1371/journal.pone.0129466

Cited by 4 publications

(3 citation statements)

References 27 publications

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“…have shown that the expression levels of PGE2 and EP1/2 mRNA are significantly higher in BPS/IC patients4. Several studies have also suggested that the PGE2/EP1/EP2 pathway is involved in the development of BPS/IC416. Importantly, the results of Takahashi’s study showed that PGE2 can regulate the expression of ICAM-1 via the EP2 receptor17.…”

Section: Discussionmentioning

confidence: 99%

Specific inhibition of ICAM-1 effectively reduces bladder inflammation in a rat model of severe non-bacterial cystitis

Zhang

et al. 2016

Sci Rep

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The development and progression of bladder pain syndrome/interstitial cystitis (BPS/IC) is closely related to bladder inflammation. Intercellular adhesion molecule 1 (ICAM-1) is associated with bladder inflammation in BPS/IC. We investigated the effect of specific inhibition of ICAM-1 using an anti-ICAM-1 antibody (AIA) on bladder inflammation in a rat model of severe non-bacterial cystitis (NBC) resembling BPS/IC by evaluating the bladder inflammation grade, mast cell infiltration and related cytokines and receptors. We also compared the effects of AIA with the COX-2 inhibitor celecoxib and the neurokinin-1 receptor (NK1R) inhibitor aprepitant. Our NBC model was established by intraperitoneal injection of cyclophosphamide combined with intravesical protamine/lipopolysaccharide, which resulted in severe bladder inflammation and increased mast cell infiltration, similar to the pathological changes of BPS/IC. Inhibition of ICAM-1 by AIA significantly decreased the bladder inflammation grade and mast cell counts, which was accompanied by a reduction of purinergic receptors (P2X2/P2X3), prostaglandin E2, EP1/EP2 receptors, TNF-α, NK1R, and ICAM-1. Moreover, AIA showed superior effects to those of celecoxib and aprepitant treatment in improving the bladder inflammatory response. Our results suggest that ICAM-1 may play a critical role in bladder inflammation in severe NBC and may be used as a novel therapeutic target in non-bacterial bladder inflammation such as BPS/IC.

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Section: Discussionmentioning

confidence: 99%

Specific inhibition of ICAM-1 effectively reduces bladder inflammation in a rat model of severe non-bacterial cystitis

Zhang

et al. 2016

Sci Rep

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“…В клетках толстого восходящего отдела петли Генле они снижают реабсорбцию ионов натрия, хлора [36] и ионов магния [37]. кроме того, у пациенток с недержанием мочи выявлена повышенная экскреция простаглан-дина е 2 с мочой [38][39][40].…”

Section: обсуждение результатовunclassified

Experience of cyclooxygenase inhibitor use for correction of urine overproduction in incontinent women

et al. 2018

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Hypothesis/aims of study. Questions of urine incontinence pathogenesis and ways of treatment are actively discussed by gynecologists, urologists and neuropathologists. Urine incontinence often has multifactor origin: the causes of urine incontinence are connected, as a rule, with violation of urine continence functional mechanisms, anatomical and topographical features of the lower urinary tract or an age failure of ovaries function. At the same time changes of kidneys function play part in urine incontinence pathogenesis. In some cases urine incontinence is combined with urine overproduction or inversion of circadian rhythm of renal function due to decrease in a reabsorption sodium ions in the thick ascending limb of a Henle’s loop. The reabsorption of Na+, K+, Ca2+, Mg2+, Cl– in this department of a nephron is increased by vasopressin activation of V2-receptors. In some patients we succeeded to normalize ions transport, diuresis, circadian rhythm of urine production by desmopressin administration, however in some cases significant decrease in a diuresis did not happen. The lack of therapy effect could be connected with local production of substances resisting to effect of this hormone, in particular prostaglandin E2. The current analysis was undertaken to evaluate the clinical efficiency of Diclofenac in incontinent patients with nocturnal polyuria and polyuria. Study design, materials and methods. A total of 44 patients with complaints of urinary incontinence, polyuria (24-urine volume of 40 mL/kg bodyweight or above) or nocturnal polyuria (nocturnal volume/24-h urine volume of 0.33 or above) (Van Kerrebroeck P., 2002) and 14 control subjects were included. Mean patient age was 42.8 ± 4.5 years, in control subjects 39.4 ± 6.3 (p > 0.05). All participants performed 72h-urinecollection to determine the voided volumes and the levels of creatinine, osmolality, sodium, magnesium and potassium for each sample. A blood sample was taken during the 72-urinecollection to determine the levels of creatinine, osmolality, sodium, magnesium and potassium. The examination of patients with polyuria and nocturnal polyuria was performed twice: in the initial state and one month after the start of treatment with optimal dose of Diclofenac. Results. In patients with polyuria and nocturnal polyuria the glomerular filtration rate was normal, whereas diuresis and solute (sodium, magnesium, potassium) clearance in night samples in nocturnal polyuria and both in night and day samples was higher. Diclofenac use had the normalizing effect on transport of ions in a nephron.

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“…В клет-ках толстого восходящего отдела петли Генле они снижают реабсорбцию ионов Na, Cl [36] и ионов магния [37]. Кроме того, у пациенток с недержанием мочи выявлена повышенная экскреция простагландина Е 2 с мочой [38][39][40]. В группе пациенток с недержанием мочи, по-лиурией или никтурией и отсутствием эффек-та от применения десмопрессина был исполь-зован блокатор синтеза простагландинов -диклофенак натрия, что позволило добиться положительного эффекта и нормализовать ритм мочеобразования у 75,0 ± 6,5 % пациен-ток [13].…”

Section: обсуждение результатовunclassified

Clinical efficiency of desmopressin and cyclooxygenase inhibitor use in incontinent women

et al. 2018

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Hypothesis/aims of study. Questions regarding the pathogenesis of urine incontinence and methods of treatment are acti vely discussed by gynecologists, urologists, and neuropathologists. Urine incontinence often has multifactor origins: the causes of urine incontinence are connected, as a rule, with the violation of urine continence functional mechanisms, anatomotopographical features of the lower urinary tract, or an premature ovarian failure. Simultaneously, changes in kidney function play a role in the pathogenesis of urine incontinence. In some cases, urine incontinence is combined with urine overproduction or inversion of the circadian rhythm of renal function owing to a decrease in the reabsorption of sodium ions in the thick ascending limb of the loop of Henle. In some patients, we successfully normalized ion transport, diuresis, and circadian rhythm of urine production by desmopressin or diclofenac administration. The present analysis was undertaken to evaluate the clinical efficiency of desmopressin and diclofenac in incontinent patients with nocturnal polyuria and polyuria. Study design, materials, and methods. In total, 130 patients with complaints of urinary incontinence, polyuria (24-h urine volume of 40 mL/kg bodyweight or above), or nocturnal polyuria (nocturnal volume/24-h urine volume of 0.33 or above); 30 incontinent women without polyuria or nocturnal polyuria (comparison group); and 14 control subjects were included. The mean patient age was 43.6 ± 4.5 years (41.8 ± 3.7 years in the comparison group and 39.4 ± 6.3 years in the control group, p > 0.05). All the participants performed seven days of urine collection to determine the voided volumes. Patients with polyuria or nocturnal polyuria performed the 3-fold 24-h pad-test. Patients with polyuria and nocturnal polyuria were examined twice: in the initial state and one month after the start of treatment with the optimal dose of diclofenac or desmopressin (Minirin). Results. The use of both diclofenac or desmopressin in patients with various types of urine incontinence, polyuria, or nocturia decreased the volume of voided urine because of the normalization of diuresis and an increase in cystometric bladder capacity.

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Impaired Expression of Prostaglandin E2 (PGE2) Synthesis and Degradation Enzymes during Differentiation of Immortalized Urothelial Cells from Patients with Interstitial Cystitis/Painful Bladder Syndrome

Cited by 4 publications

References 27 publications

Specific inhibition of ICAM-1 effectively reduces bladder inflammation in a rat model of severe non-bacterial cystitis

Specific inhibition of ICAM-1 effectively reduces bladder inflammation in a rat model of severe non-bacterial cystitis

Experience of cyclooxygenase inhibitor use for correction of urine overproduction in incontinent women

Clinical efficiency of desmopressin and cyclooxygenase inhibitor use in incontinent women

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