Enhancement of B‐cell translocation gene‐1 expression by prostaglandin E₂ in macrophages and the relationship to proliferation

Abstract

Although prostaglandin (PG) E2 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 PGE2‐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 PGE2 treatment. PGE1 and platelet‐activating factor,but not leukotrienes B4, and C4, or lipopolysaccharide, also enhanced BTG1 expression. Furthermore, this effect was mimicked by dibutyryl cAMP which indicated the involvement of elevated cAMP in the PGE2‐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 PGE2‐mediated inhibition of macrophage proliferation and not activation.

CD47 deficiency confers cell and tissue radioprotection by activation of autophagy

“…To determine whether the lack of CD47 preserves proliferative capacity, Jurkat T cells were plated in complete medium and exposed to a 20 Gy dose of radiation. WT and CD47 − Jurkat cells showed no difference in crystal violet staining 17,18 at time 0 and similar 4-fold increases in cell numbers at day 10. On the other hand, irradiated cultures of WT cells showed only a 1.5-fold increase in proliferative capacity vs. a 4-fold increase in proliferative capacity in cells that lack CD47 (Fig.…”

“…Proliferative capacity was determined as described previously. 17,18 Briefly, 2 × 10 5 cells were plated in 24-well plates in complete media and either exposed to 10 Gy IR or left untreated as controls. Ten days after radiation treatment, cells were harvested by centrifugation, and medium was removed and the well washed with 1X PBS.…”

Role of Antiproliferative B Cell Translocation Gene-1 as an Apoptotic Sensitizer in Activation-Induced Cell Death of Brain Microglia

“…Experiments with the forced expression of the gene showed that BTG1 negatively regulates cell proliferation (16). The antiproliferative properties of BTG1 have been observed in many different cell types including PBMC (16), testis (17), and macrophages (18). Especially, in macrophages, we and others have found that the levels of BTG1 expression negatively correlate with cell proliferation (18) and that the gene expression colocalizes with an apoptotic marker (19).…”

Interaction of BTG1 and p53-regulatedBTG2 Gene Products with mCaf1, the Murine Homolog of a Component of the Yeast CCR4 Transcriptional Regulatory Complex

“…Both BTG1 and BTG2 are preferentially expressed in quiescent cells, and overexpression of these genes causes a decrease in the growth rate and clonability of NIH 3T3 cells (2). A negative correlation between BTG1 mRNA expression and cell proliferation has been observed in, for example, T lymphocytes, macrophages, and testis development (2,5,6). BTG2 is also implicated in the control of the cell cycle.…”