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[ 125 I]EGF binding ability is stable throughout the replicative life‐span of WI‐38 cells
Author(s) -
Phillips Paul D.,
Kuhnle Ellen,
Cristofalo Vincent J.
Publication year - 1983
Publication title -
journal of cellular physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.529
H-Index - 174
eISSN - 1097-4652
pISSN - 0021-9541
DOI - 10.1002/jcp.1041140309
Subject(s) - epidermal growth factor , biology , ligand (biochemistry) , receptor , in vitro , degradation (telecommunications) , thymidine , cell culture , binding site , microbiology and biotechnology , life span , growth factor , dna synthesis , hormone , cell division , cell , medicine , endocrinology , biochemistry , genetics , computer science , telecommunications , evolutionary biology
Using a serum‐free medium supplemented with hormones and growth factors, which included epidermal growth factor (EGF), we investigated the binding and processing‐degradation of [ 125 I]EGF in WI‐38 cells of various in vitro ages. The binding and processing‐degradation systems of these cells remained esentially unchanged throughout their lifespan. The number of specific [ 125 I]EGF binding sites per cell increased as the cultures senesced, thought the number of specific binding sites per μm 2 (surface area) remained constant. The kinetics of ligand degradation as well as the qualitative and quantitative nature of the degradation products also remained essentially unchanged throughout the life‐span. The only consistent alteration in any of the binding parameters measured was the slight decrease in the apparent k d of the ligand‐receptor complex, independent of temperature. Quantitation of EGF‐stimulated DNA synthesis revealed a decrease in the percentage of cells incorporating [ 3 H]thymidine ([ 3 H]TdR) during a 30‐h exposure from 45% in young cells to 0.25% in senescent cells, although [ 125 I]EGF binding or processing‐degradation did not differ significantly in yong and old cells. Thus, EGF binding does not decrease in senescence.