FIB-SEM and automatic segmentation for investigation of mitochondrial organization in umbrella cells of the urinary bladder urothelium

2021 ◽  
Author(s):  
Rok Romih ◽  
2020 ◽  
Author(s):  
Zane Stromberga ◽  
Russ Chess-Williams ◽  
Christian Moro

Abstract Background: Inflammation is often associated with several bladder dysfunctions, including overactive bladder (OAB) and interstitial cystitis/bladder pain syndrome (IC/PBS). As such, inflammation of the bladder and the actions of inflammatory mediators may contribute to the development of the urinary symptoms. This study assessed the actions of PGE 2 , PGF 2 , PGD 2 , TXA 2 , and PGI 2 on the urinary bladder urothelium with lamina propria (U&LP), as well as the detrusor smooth muscle.Methods: Studies were carried out using isolated tissue baths, where strips porcine bladder U&LP or detrusor were exposed to varying concentrations of prostaglandin agonists (1 µM and 10 µM).Results: All assessed prostaglandin agonists contracted both the U&LP and detrusor smooth muscle, with the rank order of contractile response effectiveness as: PGE 2 > PGF 2α > TXA 2 > PGD 2 > PGI 2 . In U&LP, treatment with PGE 2 (10 µM) increased tonic contractions by 1.36 ± 0.09 g (n = 42, p < 0.001) and phasic contractions by 40.4 ± 9.6% (n = 42, p < 0.001). In response to PGF 2α (10 µM), U&LP tonic contractions increased by 0.79 ± 0.06 g (n = 14, p < 0.001) and phasic activity by 13.3% ± 5.3% (n = 15, p < 0.05). In detrusor preparations, PGE 2 (10 µM) increased tonic contractions by 1.32 ± 0.13 g (n = 38, p < 0.001) and PGF 2α (10 µM) by 0.97 ± 0.14 g (n = 12, p < 0.001). Only 34% (n = 48) of all detrusor preparations exhibited spontaneous activity prior to the addition of any agonist at a frequency of 2.03 ± 0.12 cpm. In preparations that did not exhibit initial phasic activity, all of the prostaglandin agonists were capable of commencing phasic activity.Conclusions: The urinary bladder U&LP and detrusor respond to a variety of prostaglandin agonists, with their activation resulting in direct contractions, as well as increases to spontaneous contractile activity. This study presents the prostaglandin receptor system as a potential therapeutic target for lower urinary tract dysfunction.


2005 ◽  
Vol 33 (5) ◽  
pp. 552-560 ◽  
Author(s):  
Martin B. Oleksiewicz ◽  
Inger Thorup ◽  
Henriette S. Nielsen ◽  
Hanne V. Andersen ◽  
Anne Charlotte Hegelund ◽  
...  

2005 ◽  
Vol 562 (3) ◽  
pp. 859-871 ◽  
Author(s):  
Bikramjit Chopra ◽  
Stacey R. Barrick ◽  
Susan Meyers ◽  
Jonathan M. Beckel ◽  
Mark L. Zeidel ◽  
...  

1983 ◽  
Vol 96 (6) ◽  
pp. 1662-1670 ◽  
Author(s):  
G R Cunha ◽  
H Fujii ◽  
B L Neubauer ◽  
J M Shannon ◽  
L Sawyer ◽  
...  

Tissue recombinants of embryonic urogenital sinus mesenchyme (UGM) and epithelium of the urinary bladder (urothelium, BLE) of adult rats and mice were grown for 3-30 d in male syngeneic hosts. Short-term in vivo growth indicated that prostatic morphogenesis is initiated as focal outgrowths from the basal aspect of the adult urothelium. The solid epithelial buds elongate, branch, and subsequently canalize, forming prostatic acini. After 30 d of growth in the male hosts, prostatic acini exhibit secretory activity. The marked changes in urothelial morphology induced by the UGM are accompanied by the expression of fine-structural features indicative of secretory function (rough endoplasmic reticulum, Golgi apparatus, and secretory granules). During this process, urothelial cells express prostatic histochemical markers (alkaline phosphatase, nonspecific esterase, glycosaminoglycans) and prostate-specific antigens. The expression within BLE of prostatic characteristics is associated with the loss of urothelial characteristics. These data indicate that adult urothelial cells retain a responsiveness to embryonic mesenchymal inductors. Furthermore, mesenchyme-induced changes in urothelial cytodifferentiation appear to be coupled to changes in functional activity.


2012 ◽  
Vol 23 (7) ◽  
pp. 1354-1366 ◽  
Author(s):  
Ge Zhou ◽  
Feng-Xia Liang ◽  
Rok Romih ◽  
Zefang Wang ◽  
Yi Liao ◽  
...  

The apical surface of mammalian bladder urothelium is covered by large (500–1000 nm) two-dimensional (2D) crystals of hexagonally packed 16-nm uroplakin particles (urothelial plaques), which play a role in permeability barrier function and uropathogenic bacterial binding. How the uroplakin proteins are delivered to the luminal surface is unknown. We show here that myelin-and-lymphocyte protein (MAL), a 17-kDa tetraspan protein suggested to be important for the apical sorting of membrane proteins, is coexpressed with uroplakins in differentiated urothelial cell layers. MAL depletion in Madin–Darby canine kidney cells did not affect, however, the apical sorting of uroplakins, but it decreased the rate by which uroplakins were inserted into the apical surface. Moreover, MAL knockout in vivo led to the accumulation of fusiform vesicles in mouse urothelial superficial umbrella cells, whereas MAL transgenic overexpression in vivo led to enhanced exocytosis and compensatory endocytosis, resulting in the accumulation of the uroplakin-degrading multivesicular bodies. Finally, although MAL and uroplakins cofloat in detergent-resistant raft fractions, they are associated with distinct plaque and hinge membrane subdomains, respectively. These data suggest a model in which 1) MAL does not play a role in the apical sorting of uroplakins; 2) the propensity of uroplakins to polymerize forming 16-nm particles and later large 2D crystals that behave as detergent-resistant (giant) rafts may drive their apical targeting; 3) the exclusion of MAL from the expanding 2D crystals of uroplakins explains the selective association of MAL with the hinge areas in the uroplakin-delivering fusiform vesicles, as well as at the apical surface; and 4) the hinge-associated MAL may play a role in facilitating the incorporation of the exocytic uroplakin vesicles into the corresponding hinge areas of the urothelial apical surface.


2001 ◽  
Vol 115 (4) ◽  
pp. 309-316 ◽  
Author(s):  
Andreja Erman ◽  
Kristijan Jezernik ◽  
Draga Štiblar-Martinčič ◽  
Rok Romih ◽  
Peter Veranič

2003 ◽  
Vol 284 (5) ◽  
pp. F966-F976 ◽  
Author(s):  
Gerard Apodaca ◽  
Susanna Kiss ◽  
Wily Ruiz ◽  
Susan Meyers ◽  
Mark Zeidel ◽  
...  

Neural-epithelial interactions are hypothesized to play an important role in bladder function. We determined whether spinal cord injury (SCI) altered several indicators of urinary bladder epithelium barrier function, including continuity of the surface umbrella cell layer, transepithelial resistance (TER), and urea and water permeability. Within 2 h of SCI, significant changes in uroepithelium were noted, including disruption of the surface umbrella cells and an ∼50% decrease in TER. By 24 h, TER reached a minimum and was accompanied by significant increases in water and urea permeability. Regeneration of the surface uroepithelium was accomplished by 14 days after SCI and was accompanied by a return to normal TER and urea and water permeabilities. This early disruption of the uroepithelial permeability and accompanying changes in uroepithelial morphology were prevented by pretreatment with hexamethonium (a blocker of ganglion transmission), indicating involvement of sympathetic or parasympathetic input to the urinary bladder. In addition, prior treatment with capsaicin worsened the effect of SCI on uroepithelial permeability, suggesting that capsaicin-sensitive afferents may play a protective role in the process. These results demonstrate that SCI results in a significant disruption of the urinary bladder uroepithelium and that these changes may be mediated in part by an interaction with bladder nerves.


Author(s):  
Alina Romanenko ◽  
Keiichirou Morimura ◽  
Hideki Wanibuchi ◽  
Elsayed I. Salim ◽  
Anna Kinoshita ◽  
...  

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