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Expression of Transgenes in Native Bladder Urothelium Using Adenovirus-Mediated Transduction
Published on: October 6, 2022
Uroplakins do not restrict CO2 transport through urothelium
Florian Zocher1, Mark L Zeidel, Andreas Missner
1Institut für Biophysik, Johannes Kepler Universität, 4020 Linz, Austria.
The Journal of Biological Chemistry
|February 9, 2012
Summary
The bladder
Area of Science:
- Physiology
- Membrane Biology
- Biophysics
Background:
- Partial carbon dioxide (CO2) pressure in urine is higher than in blood, suggesting a bladder permeability barrier.
- Uroplakin complexes in umbrella cell apical membranes are hypothesized to be responsible for this CO2 barrier.
Purpose of the Study:
- To investigate the permeability barrier to CO2 in the bladder epithelium.
- To determine if carbonic anhydrase (CA) activity influences CO2 transport across biological membranes.
Main Methods:
- Disruption of uroplakin layer in mouse bladders to assess water, urea, and CO2 permeability.
- Measurement of carbonic anhydrase (CA) activity in bladder epithelium.
- Experiments on Madin-Darby canine kidney (MDCK) cell monolayers with and without CA to determine CO2 permeability (P(CO2)).
Main Results:
- Disrupting the urothelium increased water and urea permeability but did not affect bladder P(CO2).
- Bladder epithelium lacks carbonic anhydrase (CA) activity.
- In MDCK cells, P(CO2) was unstirred layer limited with CA but limited by CO2 hydration kinetics without CA, showing a 14-fold decrease.
- Aquaporin-1 expression did not alter P(CO2).
Conclusions:
- The urinary bladder's low CO2 permeability is attributed to the absence of carbonic anhydrase (CA).
- CO2 transport across biological membranes is significantly influenced by CA activity, suggesting a regulatory mechanism for membrane tightness to CO2.
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