Modulation of intracellular potassium and ATP: effects on coated pit function in fibroblasts and hepatocytes.
Previously we reported that cultured human fibroblasts depleted of intracellular potassium (K+) had a reduced number of surface coated pits and were unable to internalize receptor-bound molecules such as low density lipoprotein (LDL). We have extended these studies in two important ways. First, we have developed a method for modulating the number of coated pits in situ. Human fibroblasts incubated in K+-free buffer that contains 4 micron nigericin rapidly become depleted of K+ and lose the ability to internalize 125I-LDL. When rat livers are perfused with the same buffer, there is a 75% decrease in the number of surface coated pits in hepatocytes. Secondly, we have explored the possibility that K+-depletion effects coated pit function by lowering intracellular ATP. We found that although this protocol lowers intracellular ATP by 40-70%, when ATP concentrations are lowered greater than 95% by metabolic inhibitors, receptor-mediated endocytosis is unaffected.
Larkin
J M
JM
Donzell
W C
WC
Anderson
R G
RG
D000255:Adenosine Triphosphate / Q000378:metabolism*; D000818:Animals; D001706:Biopsy; D003034:Coated Pits, Cell-Membrane / Q000502:physiology*; D004705:Endocytosis; D011992:Endosomes / Q000502:physiology*; D005347:Fibroblasts / Q000648:ultrastructure*; D006801:Humans; D008077:Lipoproteins, LDL / Q000378:metabolism; D008099:Liver / Q000648:ultrastructure*; D008854:Microscopy, Electron; D009550:Nigericin / Q000494:pharmacology; D011188:Potassium / Q000378:metabolism*; D051381:Rats; D011919:Rats, Inbred Strains; D012867:Skin / Q000166:cytology
D008077:Lipoproteins, LDL; D000255:Adenosine Triphosphate; D009550:Nigericin; D011188:Potassium