Abstract
HeLa cells express low levels of β-adrenergic receptor (βAR) of the β2-subtype. When exposed to sodium butyrate, receptor levels increased up to 4-fold in a time dependent manner, reaching a maximum after 12 to 15 h of treatment. Sodium butyrate treatment also caused a 3 to 4 fold increase in levels of β2AR mRNA determined by hybridization blot analysis. The induction of β2AR mRNA temporally preceded the increase in receptor binding activity, reaching a maximum after 4 to 6 h of treatment, and remaining elevated for up to 24 h. Prior exposure of the cells to the protein synthesis inhibitor cycloheximide prevented the butyrate-induced increase in receptor binding but had no effect on the increase in receptor mRNA. Blocking DNA synthesis and cell growth by excess thymidine did not increase β2AR mRNA or binding or prevent the effects of sodium butyrate. Thus, butyrate appears to induce βAR mRNA by a mechanism independent of DNA and protein synthesis.