Publication: UTP-dependent inhibition of Na+ absorption requires activation of PKC in endometrial epithelial cells
0
0
Issued Date
2002
Resource Type
File Type
application/pdf
ISSN
221295
Other identifier(s)
2-s2.0-1842856100
Rights Holder(s)
Scopus
Bibliographic Citation
Journal of General Physiology. Vol 120, No.6 (2002), p.897-906
Suggested Citation
Palmer-Densmore M., Deachapunya C., Kannan M., O'Grady S.M. UTP-dependent inhibition of Na+ absorption requires activation of PKC in endometrial epithelial cells. Journal of General Physiology. Vol 120, No.6 (2002), p.897-906. doi:10.1085/jgp.20028608 Retrieved from: https://hdl.handle.net/20.500.14740/6678
Abstract
The objective of this study was to investigate the mechanism of uridine 5′-triphosphate (UTP)-dependent inhibition of Na+ absorption in porcine endometrial epithelial cells. Acute stimulation with UTP (5 μM) produced inhibition of sodium absorption and stimulation of chloride secretion. Experiments using basolateral membrane-permeabilized cell monolayers demonstrated a reduction in benzamil-sensitive Na+ conductance in the apical membrane after UTP stimulation. The UTP-dependent inhibition of sodium transport could be mimicked by PMA (1 μM). Several PKC inhibitors, including GF109203X and Gö6983 (both nonselective PKC inhibitors) and rottlerin (a PKCδ selective inhibitor), were shown to prevent the UTP-dependent decrease in benzamil-sensitive current. The PKCα-selective inhibitors, Gö6976 and PKC inhibitor 20-28, produced a partial inhibition of the UTP effect on benzamil-sensitive Isc. Inhibition of the benzamil-sensitive Isc by UTP was observed in the presence of BAPTA-AM (50 μM), confirming that activation of PKCs, and not increases in [Ca2+]i, were directly responsible for the inhibition of apical Na+ channels and transepithelial Na+ absorption.
Subject(s)
12 (2 cyanoethyl) 6,7,12,13 tetrahydro 13 methyl 5 oxoindolo[2,3 a]pyrrolo[3,4 c]carbazole
2 [1 (3 dimethylaminopropyl) 3 indolyl] 3 (3 indolyl)maleimide
2 [1 (3 dimethylaminopropyl) 5 methoxy 1h indol 3 yl] 3 (1h indol 3 yl)maleimide
Benzamil
Calcium ion
Chloride ion
Ethylene glycol 1,2 bis(2 aminophenyl) ether n,n,n',n' tetraacetic acid
Phorbol 13 acetate 12 myristate
Protein kinase C
Protein kinase C inhibitor
Sodium channel
Sodium ion
Uridine triphosphate
Carrier protein
Protein kinase C
Protein kinase modulator
Signal peptide
Sodium
Uridine triphosphate
Animal cell
Article
Calcium activated sodium channel
Cell membrane permeability
Cell secretion
Controlled study
Endometrium
Enzyme activation
Epithelium cell
Nonhuman
Sodium absorption
Sodium conductance
Swine
Absorption
Animal
Cytology
Drug antagonism
Drug effect
Enzyme activation
Enzymology
Female
Metabolism
Physiology
Absorption
Animals
Carrier Proteins
Endometrium
Enzyme Activation
Epithelial Cells
Female
Intracellular Signaling Peptides and Proteins
Protein Kinase C
Sodium
Swine
Uridine Triphosphate
2 [1 (3 dimethylaminopropyl) 3 indolyl] 3 (3 indolyl)maleimide
2 [1 (3 dimethylaminopropyl) 5 methoxy 1h indol 3 yl] 3 (1h indol 3 yl)maleimide
Benzamil
Calcium ion
Chloride ion
Ethylene glycol 1,2 bis(2 aminophenyl) ether n,n,n',n' tetraacetic acid
Phorbol 13 acetate 12 myristate
Protein kinase C
Protein kinase C inhibitor
Sodium channel
Sodium ion
Uridine triphosphate
Carrier protein
Protein kinase C
Protein kinase modulator
Signal peptide
Sodium
Uridine triphosphate
Animal cell
Article
Calcium activated sodium channel
Cell membrane permeability
Cell secretion
Controlled study
Endometrium
Enzyme activation
Epithelium cell
Nonhuman
Sodium absorption
Sodium conductance
Swine
Absorption
Animal
Cytology
Drug antagonism
Drug effect
Enzyme activation
Enzymology
Female
Metabolism
Physiology
Absorption
Animals
Carrier Proteins
Endometrium
Enzyme Activation
Epithelial Cells
Female
Intracellular Signaling Peptides and Proteins
Protein Kinase C
Sodium
Swine
Uridine Triphosphate