Modulation of membrane receptor endocytosis by chemical effectors of membrane fluidity.
Several chemical effectors were used to induce changes in spleen B cell membrane fluidity. Membrane fluidity was monitored by fluorescence polarization analysis of the hydrophobic probe 1,6-diphenyl-1,3,5-hexatriene (DPH) and cell viability was checked not to be affected by the treatments. Membrane immunoglobulin (Ig) endocytosis by the living B cells with modified or unmodified membranes was quantitatively measured by flow cytometry, using a previously described method (Métézeau et al., 1982, 1984). The kinetics of endocytosis of membrane Ig was not affected by chemical effectors increasing membrane fluidity. On the contrary, increasing membrane microviscosity resulted in the slowing down and eventually the blocking of membrane Ig endocytosis. It is suggested that a step depending on membrane microviscosity is involved in the process of endocytosis; this step may become rate limiting when membranes are artificially rendered or naturally become (i.e. for pathological or particularly differentiated cells) more viscous.
D000818:Animals; D001402:B-Lymphocytes / Q000166:cytology / Q000276:immunology* / Q000378:metabolism; D002462:Cell Membrane / Q000378:metabolism*; D002470:Cell Survival; D002788:Cholesterol Esters / Q000378:metabolism; D004161:Diphenylhexatriene; D004705:Endocytosis; D005434:Flow Cytometry; D007136:Immunoglobulins / Q000378:metabolism*; D008081:Liposomes; D008297:Male; D008560:Membrane Fluidity / Q000187:drug effects*; D008563:Membrane Lipids / Q000378:metabolism; D051379:Mice; D008815:Mice, Inbred Strains; D010743:Phospholipids / Q000378:metabolism / Q000494:pharmacology*
D002788:Cholesterol Esters; D007136:Immunoglobulins; D008081:Liposomes; D008563:Membrane Lipids; D010743:Phospholipids; D004161:Diphenylhexatriene; C013440:cholesteryl succinate