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CYSTIC FIBROSIS AND NORMAL FIBROBLASTS HAVE IDENTICAL GLUCOCORTICOID RECEPTOR PROFILES AND INDUCED PROTEIN RESPONSES
Author(s) -
KHALID B. A. K.,
GYORKI S.,
WARNE G. L.,
FUNDER J. W.
Publication year - 1983
Publication title -
clinical endocrinology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.055
H-Index - 147
eISSN - 1365-2265
pISSN - 0300-0664
DOI - 10.1111/j.1365-2265.1983.tb00586.x
Subject(s) - cystic fibrosis , endocrinology , medicine , glucocorticoid , glucocorticoid receptor , dexamethasone , receptor , fibrosis , biology , chemistry
SUMMARY The possibility of differences in glucocorticoid sensitivity between normal and cystic fibrosis fibroblasts was studied in cultured cells derived from forearm skin biopsies. Both normal and cystic fibrosis cells bound tritiated dexamethasone with high affinity ( K d 37°C ± 10 nmol/l) to a limited class of sites (concentration ± 50,000/cell); no difference between cystic fibrosis and normal cells was seen in the nuclear transfer of receptor‐bound tritiated dexamethasone. After 4 h exposure to dexamethasone and analysis of 35 S‐methionine labelled proteins by 2‐dimensional gel electrophoresis, both normal and cystic fibrosis cells showed increased abundance of protein kappa (molecular weight ∼ 41,000; p K i ∼6.5) over non‐steroid exposed gels. After 16 h exposure, in both cystic fibrosis and normal cells exposed to dexamethasone a decrease in protein omega (mol. wt ∼ 42,000; p K i ∼ 5.4) was seen compared with control. We interpret these data as evidence against a difference in glucocorticoid receptor or effector mechanisms between cystic fibrosis and normal fibroblasts.