Depletion of intracellular potassium arrests coated pit formation and receptor-mediated endocytosis in fibroblasts

Janet M. Larkin, Michael S. Brown, Joseph L. Goldstein, Richard G W Anderson

Research output: Contribution to journalArticle

325 Scopus citations

Abstract

Depletion of intracellular potassium (K+) caused a marked reduction in the rate of endocytosis of receptor-bound low density lipoprotein (LDL) and epidermal growth factor (EGF) in human fibroblasts. K+ could be depleted slowly by a 3-hr incubation of cells in isotonic K+-free buffer. Rapid K+ depletion was induced by incubation of cells for 5 min with hypotonic medium, followed by transfer to isotonic K+-free buffer. Within 30 min of this treatment, cellular K+ levels fell by more than 60%. When the K+ level fell below a threshold of 40% of normal, the number of coated pits declined by 80% and the rate of endocytosis of 125I-LDL decreased by 70 to 95% despite normal to increased receptor binding. Similar results were obtained with 125I-epidermal growth factor. Addition of KCI to the culture medium up to 2 hr after K+ depletion restored cellular K+ levels and returned endocytosis of 125I-LDL promptly to normal. RbCl was as effective as KCl, but CsCl, LiCI, and (CH3)4NCI had no effect. Restoration by KCI was blocked by ouabain, indicating that uptake via the Na+/K+ ATPase was required. These data demonstrate that depletion of intracellular K+ reversibly arrests coated pit formation and receptor-mediated endocytosis in human fibroblasts.

Original languageEnglish (US)
Pages (from-to)273-285
Number of pages13
JournalCell
Volume33
Issue number1
DOIs
StatePublished - May 1983

ASJC Scopus subject areas

  • Biochemistry, Genetics and Molecular Biology(all)

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