Cell Surface Changes in Senescent and Werner’s Syndrome Fibroblasts: Their Role in Cell Proliferation
Werner’s syndrome (WS) has segmental progeroid features and pedigree analysis suggests its autosomal recessive inheritance (Epstein et al., 1966). Two of the clinical characteristics of Werner’s syndrome are hyperkeratinized skin and an excessive excretion of hyaluronic acid into the urine (Tokuraga et al., 1975, Goto and Murata, 1978) suggesting some disorder(s) of connective-tissue metabolism. Cultured fibroblasts from human skin have been used for characterization of genetic defects in many inherited diseases. Epstein et al. (1966) cultured fibroblast-like cells from the skin of patients with WS and noted that they grew very poorly. Since then, WS fibroblasts have been used to find the explanation for the shortened lifespan in vivo and in vitro (Martin et al., 1970). However, the primary molecular defect that retards cell growth has remained elusive. Recently, Salk (1982) published an extensive review article summarizing 15 years of research since that of Epstein et al.
KeywordsCellulose Migration Fermentation EDTA Electrophoresis
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