Maitotoxin stimulates Cd influx in Madin-Darby kidney cells by activating Ca-permeable cation channels

L. Olivi, Joseph Bressler

Research output: Contribution to journalArticle

Abstract

This study examined the role of calcium channels for the uptake of cadmium (Cd) into Madin-Darby canine kidney (MDCK) cells. Maitotoxin, an activator of different types of calcium channels, increased accumulation of 109Cd and 45Ca in MDCK cells. We found that maitotoxin increased accumulation by stimulating 109Cd influx because it did not affect efflux. An inhibitor of store-operated Ca channels, SKF96365, partially blocked 45Ca influx but did not affect 109Cd influx. Ni and Mn, and loperamide and proadifen (SKF 525a), inhibited 45Ca and 109Cd influx in cells stimulated with maitotoxin, but La and nifedipine did not. Overnight treatment with phorbol 12, 13-ibutyrate (PDBu) to activate protein kinase C resulted in a decrease in the concentration of maitotoxin needed to stimulate 45Ca and 109Cd influx. The effect of PDBu was blocked by treating cells with the protein kinase C inhibitor GF109203X. Additionally, the effect of PDBu was lost in cells treated with an inhibitor of RNA synthesis actinomycin D. These results suggest that a Ca permeable cation channel different from voltage-dependent and store-operated Ca channels mediates the uptake of Cd in MDCK cells. The expression of this channel is regulated by protein kinase C. (C) 2000 Harcourt Publishers Ltd.

Original languageEnglish (US)
Pages (from-to)187-193
Number of pages7
JournalCell Calcium
Volume27
Issue number4
DOIs
StatePublished - Apr 2000

Fingerprint

Cadmium
Madin Darby Canine Kidney Cells
Cations
Proadifen
Protein Kinase C
Kidney
1-(2-(3-(4-methoxyphenyl)propoxy)-4-methoxyphenylethyl)-1H-imidazole
Calcium Channel Agonists
Loperamide
Nucleic Acid Synthesis Inhibitors
Protein C Inhibitor
Dactinomycin
Calcium Channels
Nifedipine
Protein Kinase Inhibitors
maitotoxin

ASJC Scopus subject areas

  • Cell Biology
  • Endocrinology

Cite this

Maitotoxin stimulates Cd influx in Madin-Darby kidney cells by activating Ca-permeable cation channels. / Olivi, L.; Bressler, Joseph.

In: Cell Calcium, Vol. 27, No. 4, 04.2000, p. 187-193.

Research output: Contribution to journalArticle

@article{9ca6f0dbad964387b0197975b89e53b5,
title = "Maitotoxin stimulates Cd influx in Madin-Darby kidney cells by activating Ca-permeable cation channels",
abstract = "This study examined the role of calcium channels for the uptake of cadmium (Cd) into Madin-Darby canine kidney (MDCK) cells. Maitotoxin, an activator of different types of calcium channels, increased accumulation of 109Cd and 45Ca in MDCK cells. We found that maitotoxin increased accumulation by stimulating 109Cd influx because it did not affect efflux. An inhibitor of store-operated Ca channels, SKF96365, partially blocked 45Ca influx but did not affect 109Cd influx. Ni and Mn, and loperamide and proadifen (SKF 525a), inhibited 45Ca and 109Cd influx in cells stimulated with maitotoxin, but La and nifedipine did not. Overnight treatment with phorbol 12, 13-ibutyrate (PDBu) to activate protein kinase C resulted in a decrease in the concentration of maitotoxin needed to stimulate 45Ca and 109Cd influx. The effect of PDBu was blocked by treating cells with the protein kinase C inhibitor GF109203X. Additionally, the effect of PDBu was lost in cells treated with an inhibitor of RNA synthesis actinomycin D. These results suggest that a Ca permeable cation channel different from voltage-dependent and store-operated Ca channels mediates the uptake of Cd in MDCK cells. The expression of this channel is regulated by protein kinase C. (C) 2000 Harcourt Publishers Ltd.",
author = "L. Olivi and Joseph Bressler",
year = "2000",
month = "4",
doi = "10.1054/ceca.1999.0115",
language = "English (US)",
volume = "27",
pages = "187--193",
journal = "Cell Calcium",
issn = "0143-4160",
publisher = "Churchill Livingstone",
number = "4",

}

TY - JOUR

T1 - Maitotoxin stimulates Cd influx in Madin-Darby kidney cells by activating Ca-permeable cation channels

AU - Olivi, L.

AU - Bressler, Joseph

PY - 2000/4

Y1 - 2000/4

N2 - This study examined the role of calcium channels for the uptake of cadmium (Cd) into Madin-Darby canine kidney (MDCK) cells. Maitotoxin, an activator of different types of calcium channels, increased accumulation of 109Cd and 45Ca in MDCK cells. We found that maitotoxin increased accumulation by stimulating 109Cd influx because it did not affect efflux. An inhibitor of store-operated Ca channels, SKF96365, partially blocked 45Ca influx but did not affect 109Cd influx. Ni and Mn, and loperamide and proadifen (SKF 525a), inhibited 45Ca and 109Cd influx in cells stimulated with maitotoxin, but La and nifedipine did not. Overnight treatment with phorbol 12, 13-ibutyrate (PDBu) to activate protein kinase C resulted in a decrease in the concentration of maitotoxin needed to stimulate 45Ca and 109Cd influx. The effect of PDBu was blocked by treating cells with the protein kinase C inhibitor GF109203X. Additionally, the effect of PDBu was lost in cells treated with an inhibitor of RNA synthesis actinomycin D. These results suggest that a Ca permeable cation channel different from voltage-dependent and store-operated Ca channels mediates the uptake of Cd in MDCK cells. The expression of this channel is regulated by protein kinase C. (C) 2000 Harcourt Publishers Ltd.

AB - This study examined the role of calcium channels for the uptake of cadmium (Cd) into Madin-Darby canine kidney (MDCK) cells. Maitotoxin, an activator of different types of calcium channels, increased accumulation of 109Cd and 45Ca in MDCK cells. We found that maitotoxin increased accumulation by stimulating 109Cd influx because it did not affect efflux. An inhibitor of store-operated Ca channels, SKF96365, partially blocked 45Ca influx but did not affect 109Cd influx. Ni and Mn, and loperamide and proadifen (SKF 525a), inhibited 45Ca and 109Cd influx in cells stimulated with maitotoxin, but La and nifedipine did not. Overnight treatment with phorbol 12, 13-ibutyrate (PDBu) to activate protein kinase C resulted in a decrease in the concentration of maitotoxin needed to stimulate 45Ca and 109Cd influx. The effect of PDBu was blocked by treating cells with the protein kinase C inhibitor GF109203X. Additionally, the effect of PDBu was lost in cells treated with an inhibitor of RNA synthesis actinomycin D. These results suggest that a Ca permeable cation channel different from voltage-dependent and store-operated Ca channels mediates the uptake of Cd in MDCK cells. The expression of this channel is regulated by protein kinase C. (C) 2000 Harcourt Publishers Ltd.

UR - http://www.scopus.com/inward/record.url?scp=0034066809&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0034066809&partnerID=8YFLogxK

U2 - 10.1054/ceca.1999.0115

DO - 10.1054/ceca.1999.0115

M3 - Article

C2 - 10858664

AN - SCOPUS:0034066809

VL - 27

SP - 187

EP - 193

JO - Cell Calcium

JF - Cell Calcium

SN - 0143-4160

IS - 4

ER -