Apical membrane area of rabbit urinary bladder increases by fusion of intracellular vesicles: An electrophysiological study

Lewis, Simon A.; Moura, J. L. C. de

doi:10.1007/bf01868937

Cited by 92 publications

(46 citation statements)

References 23 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…If extracellular ATP is a signal for pressure-induced exocytosis in umbrella cells, then depletion of extracellular ATP should inhibit exocytosis, while addition of exogenous ATP might promote exocytosis even in the absence of pressure. In the isolated uroepithelial tissue preparation used in this analysis, changes in membrane capacitance primarily reflect changes in the apical surface area of the umbrella cell layer (where 1 µF ≈ 1 cm 2 of area) and correlate well with other measures of apical exocytosis in umbrella cells (26,28,39). As shown in Figure 2, A and B, elevation of pressure caused an increase in membrane capacitance in untreated uroepithelium up to approximately 55% after 300 minutes.…”

Section: Resultsmentioning

confidence: 61%

ATP and purinergic receptor–dependent membrane traffic in bladder umbrella cells

Wang¹,

Lee²,

Ruiz³

et al. 2005

J. Clin. Invest.

208

223

View full text Add to dashboard Cite

The umbrella cells that line the bladder are mechanosensitive, and bladder filling increases the apical surface area of these cells; however, the upstream signals that regulate this process are unknown. Increased pressure stimulated ATP release from the isolated uroepithelium of rabbit bladders, which was blocked by inhibitors of vesicular transport, connexin hemichannels, ABC protein family members, and nucleoside transporters. Pressure-induced increases in membrane capacitance (a measure of apical plasma membrane surface area where 1 µF ≈ 1 cm 2 ) were inhibited by the serosal, but not mucosal, addition of apyrase or the purinergic receptor antagonist PPADS. Upon addition of purinergic receptor agonists, increased capacitance was observed even in the absence of pressure. Moreover, knockout mice lacking expression of P2X 2 and/or P2X 3 receptors failed to show increases in apical surface area when exposed to hydrostatic pressure. Treatments that prevented release of Ca 2+ from intracellular stores or activation of PKA blocked ATPγS-stimulated changes in capacitance. These results indicate that increased hydrostatic pressure stimulates release of ATP from the uroepithelium and that upon binding to P2X and possibly P2Y receptors on the umbrella cell, downstream Ca 2+ and PKA second messenger cascades may act to stimulate membrane insertion at the apical pole of these cells.

show abstract

Section: Resultsmentioning

confidence: 61%

ATP and purinergic receptor–dependent membrane traffic in bladder umbrella cells

Wang¹,

Lee²,

Ruiz³

et al. 2005

J. Clin. Invest.

208

223

View full text Add to dashboard Cite

show abstract

“…Urothelial cells undergo endo/exocytosis to modulate urothelial surface area in response to changes in bladder pressure (36), and binding of the Escherichia coli FimH receptor to UPIa mediates urothelial invasion of this bacterium (37); unlike UPIa, UPIb, or UPII, UPIIIa has a significant cytoplasmic tail, and it has been suggested that this region interacts with cytoplasmic proteins to mediate membrane/cytoplasmic interactions (25). We showed in COS-1 cells that wild-type UPIIIa protein can escape the endoplasmic reticulum and reach the cell surface only in the presence of UPIb, as was shown previously in 293T cells (23).…”

Section: Discussionmentioning

confidence: 99%

De Novo Uroplakin IIIa Heterozygous Mutations Cause Human Renal Adysplasia Leading to Severe Kidney Failure

Jenkins¹,

Bitner‐Glindzicz²,

Malcolm³

et al. 2005

Journal of the American Society of Nephrology

117

View full text Add to dashboard Cite

Human renal adysplasia usually occurs sporadically, and bilateral disease is the most common cause of childhood end-stage renal failure, a condition that is lethal without intervention using dialysis or transplantation. De novo heterozygous mutations in Uroplakin IIIa (UPIIIa) are reported in four of 17 children with kidney failure caused by renal adysplasia in the absence of an overt urinary tract obstruction. One girl and one boy in unrelated kindreds had a missense mutation at a CpG dinucleotide in the cytoplasmic domain of UPIIIa (Pro273Leu), both of whom had severe vesicoureteric reflux, and the girl had persistent cloaca; two other patients had de novo mutations in the 3 UTR (963 T3 G; 1003 T3 C), and they had renal adysplasia in the absence of any other anomaly. The mutations were absent in all sets of parents and in siblings, none of whom had radiologic evidence of renal adysplasia, and mutations were absent in two panels of 192 ethnically matched control chromosomes. UPIIIa was expressed in nascent urothelia in ureter and renal pelvis of human embryos, and it is suggested that perturbed urothelial differentiation may generate human kidney malformations, perhaps by altering differentiation of adjacent smooth muscle cells such that the metanephros is exposed to a functional obstruction of urine flow. With advances in renal replacement therapy, children with renal failure, who would otherwise have died, are surviving to adulthood. Therefore, although the mechanisms of action of the UPIIIa mutations have yet to be determined, these findings have important implications regarding genetic counseling of affected individuals who reach reproductive age.

show abstract

“…The fits had R 2 values of Ն0.98. I sc was calculated by dividing the TEV by the transepithelial electrical resistance (TER; Lewis and de Moura, 1984).…”

Section: Electrophysiological Data Acquisition and Capacitance Measurmentioning

confidence: 99%

Distinct Apical and Basolateral Membrane Requirements for Stretch-induced Membrane Traffic at the Apical Surface of Bladder Umbrella Cells

Khandelwal²,

Apodaca

2009

MBoC

127

View full text Add to dashboard Cite

Epithelial cells respond to mechanical stimuli by increasing exocytosis, endocytosis, and ion transport, but how these processes are initiated and coordinated and the mechanotransduction pathways involved are not well understood. We observed that in response to a dynamic mechanical environment, increased apical membrane tension, but not pressure, stimulated apical membrane exocytosis and ion transport in bladder umbrella cells. The exocytic response was independent of temperature but required the cytoskeleton and the activity of a nonselective cation channel and the epithelial sodium channel. The subsequent increase in basolateral membrane tension had the opposite effect and triggered the compensatory endocytosis of added apical membrane, which was modulated by opening of basolateral K ؉ channels. Our results indicate that during the dynamic processes of bladder filling and voiding apical membrane dynamics depend on sequential and coordinated mechanotransduction events at both membrane domains of the umbrella cell.

show abstract

Apical membrane area of rabbit urinary bladder increases by fusion of intracellular vesicles: An electrophysiological study

Cited by 92 publications

References 23 publications

ATP and purinergic receptor–dependent membrane traffic in bladder umbrella cells

ATP and purinergic receptor–dependent membrane traffic in bladder umbrella cells

De Novo Uroplakin IIIa Heterozygous Mutations Cause Human Renal Adysplasia Leading to Severe Kidney Failure

Distinct Apical and Basolateral Membrane Requirements for Stretch-induced Membrane Traffic at the Apical Surface of Bladder Umbrella Cells

Contact Info

Product

Resources

About