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PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2004-8-18
pubmed:abstractText
We have used the human calcium- and temperature-dependent (HaCaT) keratinocyte cell line to elucidate mechanisms of switching from a proliferating to a differentiating state. When grown in low calcium medium (<0.1 mM) HaCaT cells proliferate. However, an increase in the calcium concentration of the culture medium, [Ca(2+)](0), induces growth arrest and the cells start to differentiate. Numerous studies have already shown that the increase in [Ca(2+)](0) results in acute and sustained increases in intracellular calcium concentration, [Ca(2+)](i). We find that the Ca(2+)-induced cell differentiation of HaCaT cells is also accompanied by a significant decrease in mitochondrial membrane potential, DeltaPsi. By combining patch-clamp electrophysiological recordings and microspectrofluorimetric measurements of DeltaPsi on single cells, we show that the increase in [Ca(2+)](i) led to DeltaPsi depolarization. In addition, we report that tetraethylammonium (TEA), a blocker of plasma membrane K(+) channels, which is known to inhibit cell proliferation, and 4,4'-diisothiocyanatostilbene-2,2'-disulfonic acid (DIDS), a blocker of plasma membrane Cl(-) channels, also affect DeltaPsi. Both these agents stimulate HaCaT cell differentiation. These data therefore strongly suggest a direct causal relationship between depolarization of DeltaPsi and the inhibition of proliferation and induction of differentiation in HaCaT keratinocytes.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
1021-7770
pubmed:author
pubmed:issnType
Print
pubmed:volume
11
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
671-82
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:articleTitle
Mitochondrial membrane potential (DeltaPsi) and Ca(2+)-induced differentiation in HaCaT keratinocytes.
pubmed:affiliation
Laboratoire de Physiologie et de Physiopathologie de la Signalisation Cellulaire, Université Bordeaux 2, Bordeaux, France.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't