A NEW approach for characterizing mouse urinary pathophysiologies

Ruetten, Hannah; Henry, Gervaise H.; Liu, Teresa T.; Spratt, Heidi; Ricke, William A.; Strand, Douglas W.; Vezina, Chad M.

doi:10.14814/phy2.14964

Cited by 4 publications

(1 citation statement)

References 16 publications

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“…Length was determined by measuring the animal from the nose to the anus [ 35 ]. Bladder was measured in situ in three dimensions with a precision caliper as described [ 36 ] and bladder volume was estimated by calculating the volume of an ellipsoid in cubic millimeters [ 37 ]. The heart, spleen, left kidney, left testis and lower urinary tract were removed and fixed in 10% formalin.…”

Section: Methodsmentioning

confidence: 99%

E-cadherin deficiency promotes prostate macrophage inflammation and bladder overactivity in aged male mice

Pascal

Igarashi

Mizoguchi

et al. 2022

Aging

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Decreased E-cadherin immunostaining is frequently observed in benign prostatic hyperplasia (BPH) and was recently correlated with increased inflammation in aging prostate. Homozygous E-cadherin deletion in the murine prostate results in prostate inflammation and bladder overactivity at 6 months of age. However, this model is limited in that while E-cadherin is significantly reduced in BPH, it is not completely lost; BPH is also strongly associated with advanced age and is infrequent in young men. Here, we examined the functional consequences of aging in male mice with prostate luminal epithelial cell-specific E-cadherin heterozygosity. In control mice, aging alone resulted in an increase in prostate inflammation and changes in bladder voiding function indicative of bladder underactivity. At 24 months of age, mice with prostate-specific Cre-mediated heterozygous deletion of E-cadherin induced at 7 weeks of age developed additional prostatic defects, particularly increased macrophage inflammation and stromal proliferation, and bladder overactivity compared to age-matched control mice, which are similar to BPH/LUTS in that the phenotype is slow-progressing and age-dependent. These findings suggest that decreased E-cadherin may promote macrophage inflammation and fibrosis in the prostate and subsequent bladder overactivity in aging men, promoting the development and progression of BPH/LUTS.

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Section: Methodsmentioning

confidence: 99%

E-cadherin deficiency promotes prostate macrophage inflammation and bladder overactivity in aged male mice

Pascal

Igarashi

Mizoguchi

et al. 2022

Aging

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Evidence that methylglyoxal and receptor for advanced glycation end products are implicated in bladder dysfunction of obese diabetic ob/ob mice

Oliveira

Medeiros

Ghezzi

et al. 2023

American Journal of Physiology-Renal Physiology

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Glycolytic overload in diabetes causes large accumulation of the highly reactive dicarbonyl compound methylglyoxal (MGO) and overproduction of advanced glycation end products (AGEs), which interact with its receptors (RAGE), leading to diabetes-associated macrovascular complications. Bladder is an organ that stays most in contact with dicarbonyl species, but little is known about the importance of MGO-AGEs-RAGE pathway to diabetes-associated bladder dysfunction. Here, we aimed to investigate the role of MGO-AGEs-RAGE pathway in bladder dysfunction of diabetic male and female ob/ob mice in comparison with wild type (WT) lean mice. Diabetic ob/ob mice were treated with the AGE-breaker alagebrium (ALT-711; 1 mg/kg) for eight weeks in drinking water. Compared with WT animals, male and female ob/ob mice showed marked hyperglycemia and insulin resistance, whereas fluid intake remained unaltered. Levels of total AGEs and MGO-derived hydroimidazolone 1 (MG-H1) and RAGE in bladder tissues, as well as fluorescent AGEs in serum were significantly elevated in ob/ob mice of either sex. Collagen content was also markedly elevated in bladders of ob/ob mice. Void spot assays in filter paper in conscious mice revealed significant increases of total void volume and volume per void in ob/ob mice with no alterations of spot number. Treatment with ALT-711 significantly reduced the levels of MGO, AGEs, RAGE, and collagen content in ob/ob mice. In addition, ALT-711 treatment normalized the volume per volume and increased the number of spots in ob/ob mice. Activation of AGEs-RAGE pathways by MGO in bladder wall may contribute to pathogenesis of diabetes-associated bladder dysfunction.

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A “NEW” way to look at an “old” test: Transforming the void spot assay (VSA) into a diagnostic tool

Dalghi

2021

Physiol Rep

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A NEW approach for characterizing mouse urinary pathophysiologies

Abstract: This is an open access article under the terms of the Creat ive Commo ns Attri bution License, which permits use, distribution and reproduction in any medium, provided the original work is properly cited.

Cited by 4 publications

References 16 publications

E-cadherin deficiency promotes prostate macrophage inflammation and bladder overactivity in aged male mice

E-cadherin deficiency promotes prostate macrophage inflammation and bladder overactivity in aged male mice

Evidence that methylglyoxal and receptor for advanced glycation end products are implicated in bladder dysfunction of obese diabetic ob/ob mice

A “NEW” way to look at an “old” test: Transforming the void spot assay (VSA) into a diagnostic tool

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