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Enhancement of B‐cell translocation gene‐1 expression by prostaglandin E 2 in macrophages and the relationship to proliferation
Author(s) -
SUK K.,
SIPES D. G.,
ERICKSON K. L.
Publication year - 1997
Publication title -
immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.297
H-Index - 133
eISSN - 1365-2567
pISSN - 0019-2805
DOI - 10.1046/j.1365-2567.1997.00235.x
Subject(s) - complementary dna , macrophage , biology , gene expression , cell growth , gene , microbiology and biotechnology , lipopolysaccharide , chromosomal translocation , immunology , genetics , in vitro
Although prostaglandin (PG) E 2 is known to suppress various macrophage functions, the molecular mechanisms by which that occurs are largely unknown. To understand better those mechanisms, differential screening of a cDNA library from PGE 2 ‐treated macrophages was performed. Subsequently, the DNA sequence of a differentially expressed cDNA clone was determined and the cDNA was identified as B‐cell translocation gene‐1 (BTG1), a recently cloned antiproliferative gene. A two‐ to threefold increase in macrophage BTG1 expression was observed after PGE 2 treatment. PGE 1 and platelet‐activating factor,but not leukotrienes B 4 , and C 4 , or lipopolysaccharide, also enhanced BTG1 expression. Furthermore, this effect was mimicked by dibutyryl cAMP which indicated the involvement of elevated cAMP in the PGE 2 ‐mediated enhancement of BTG1. Moreover, there was an inverse correlation between BTG1 mRNA expression and macrophage proliferation; however, BTG1 alteration was not associated with macrophage tumoricidal activation. Thus, BTG1 may play a role in PGE 2 ‐mediated inhibition of macrophage proliferation and not activation.