[The intracellular degradation of 125I-EGF and the release of low-molecular degradation products under conditions of actin cytoskeleton disorganization].
The influence of cytochalasin B (CB) on the epidermal growth factor (EGF) intracellular degradation and release of low-molecular products of degradation into the culture medium were investigated using two cell lines, A431 and 3T3. Investigated parameters were registered 3.0-4.5 h after the beginning of 125I-EGF endocytosis at 37 degrees C. With A431 cells it was shown that actin cytoskeleton disorganization significantly reduced the rate of 125I-EGF final degradation: a high amount of 125I-EGF, still retained cell-associated, and a reduced amount of low-molecular degradation products were released into the medium in experiments with CB addition. That is in agreement with our previous results (Barkan et al., 1988), revealing a long-term accumulation of EGF-rhodamine fluorescence in a juxtanuclear area of A431 cells after CB treatment. Nevertheless when similar experiments were performed on Swiss 3T3 cells, previously used as a model for demonstrating the inhibitory effect of CB on DNA synthesis stimulation by EGF (Barkan, Nikol'skiĭ, 1986), we could not find such a distinct influence of CB on the process of degradation of internalised 125I-EGF.
Barkan
R S
RS
Alekseev
V Iu
VIu
D016475:3T3 Cells / Q000187:drug effects / Q000378:metabolism; D000199:Actins / Q000187:drug effects / Q000378:metabolism*; D000818:Animals; D003571:Cytochalasin B / Q000494:pharmacology; D003599:Cytoskeleton / Q000187:drug effects / Q000378:metabolism*; D004815:Epidermal Growth Factor / Q000032:analysis / Q000187:drug effects / Q000378:metabolism*; D006801:Humans; D007457:Iodine Radioisotopes; D051379:Mice; D008970:Molecular Weight; D013997:Time Factors; D014407:Tumor Cells, Cultured / Q000187:drug effects / Q000378:metabolism
D000199:Actins; D007457:Iodine Radioisotopes; D003571:Cytochalasin B; D004815:Epidermal Growth Factor
Vnutrikletochnaia degradatsiia 125I-EFR i vyvedenie nizkomolekuliarnykh produktov degradatsii v usloviiakh dezorganizatsii aktinovogo tsitoskeleta.