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  3. Down-Regulation of Annexin A1 in the Urothelium Decreases Cell Survival After Bacterial Toxin Exposure
 

Down-Regulation of Annexin A1 in the Urothelium Decreases Cell Survival After Bacterial Toxin Exposure

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BORIS DOI
10.7892/boris.50042
Date of Publication
July 2013
Publication Type
Article
Division/Institute

Departement Klinische...

Institut für Anatomie...

Institut für Anatomie...

Universitätsklinik fü...

Author
Monastyrskaya-Stäuber, Katia
Departement Klinische Forschung, Forschungsgruppe Urologie
Babiichuk, Eduard
Institut für Anatomie, Zellbiologie
Draeger, Annette
Institut für Anatomie
Burkhard, Fiona Christine
Universitätsklinik für Urologie
Subject(s)

600 - Technology::610...

Series
Journal of urology
ISSN or ISBN (if monograph)
0022-5347
Publisher
Elsevier
Language
English
Publisher DOI
10.1016/j.juro.2013.01.088
PubMed ID
23376147
Uncontrolled Keywords

urinary bladder

urothelium

pain

annexins

cell differentiation

Description
PURPOSE:

We examined the role of annexins in bladder urothelium. We characterized expression and distribution in normal bladders, biopsies from patients with bladder pain syndrome, cultured human urothelium and urothelial TEU-2 cells.

MATERIALS AND METHODS:

Annexin expression in bladder layers was analyzed by quantitative reverse transcriptase-polymerase chain reaction and immunofluorescence. We assessed cell survival after exposure to the pore forming bacterial toxin streptolysin O by microscopy and alamarBlue® assay. Bladder dome biopsies were obtained from 8 asymptomatic controls and 28 patients with symptoms of bladder pain syndrome.

RESULTS:

Annexin A1, A2, A5 and A6 were differentially distributed in bladder layers. Annexin A6 was abundant in detrusor smooth muscle and low in urothelium, while annexin A1 was the highest in urothelium. Annexin A2 was localized to the lateral membrane of umbrella cells but excluded from tight junctions. TEU-2 cell differentiation caused up-regulation of annexin A1 and A2 and down-regulation of annexin A6 mRNA. Mature urothelium dedifferentiation during culture caused the opposite effect, decreasing annexin A1 and increasing annexin A6. Annexin A2 influenced TEU-2 cell epithelial permeability. siRNA mediated knockdown of annexin A1 in TEU-2 cells caused significantly decreased cell survival after streptolysin O exposure. Annexin A1 was significantly reduced in biopsies from patients with bladder pain syndrome.

CONCLUSIONS:

Several annexins are expressed in human bladder and TEU-2 cells, in which levels are regulated during urothelial differentiation. Annexin A1 down-regulation in patients with bladder pain syndrome might decrease cell survival and contribute to compromised urothelial function.
Handle
https://boris-portal.unibe.ch/handle/20.500.12422/121801
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Monastyrskaya_J%20Urol_2013_190_325.pdftextAdobe PDF3.03 MBpublisherpublished restricted
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