Modulation of thymocyte apoptosis by isoproterenol and prostaglandin E2

Induction of cyclo-oxygenase-2 mRNA by prostaglandin E2 in human prostatic carcinoma cells

“…Furthermore, PGE2 has recently been implicated in the growth and differentiation of human B-lymphocytes activated through their CD40 antigen (Garrone et al, 1994). In spite of the evidence that PGE2 can act as a growth regulator, other data have demonstrated that high levels of PGE2 can cause growth arrest and, potentially, programmed cell death in a number of primary and established cell lines of immunological origins, such as thymocytes (Suzuki et al, 1991) and B-lymphocytes (Brown et al, 1992). We, however, did not find any evidence that dmPGE2, at the concentrations used in this paper (as described in Materials and methods), promotes cell death in PC-3 cells.…”

Sympathetic modulation of immunity: Relevance to disease

“…Similarly, catecholamines or isoproterenol decrease concanavalin A (Con A)-or LPS-induced proliferation of murine thymocytes, an effect not observed with α-AR agonist treatment [65]. Although there are no reports directly relating β-AR stimulation and the induction of apoptosis, studies have demonstrated that elevating thymocyte intracellular cAMP induces apoptosis [66][67][68]. Thymocyte proliferation increases with treatment with high concentrations of either EPI or isoproterenol [69] or low concentrations of NE.…”

Exclusive expression of the Gs‐linked prostaglandin E2 receptor subtype 4 mRNA in human mononuclear Jurkat and KM‐3 cells and coexpression of subtype 4 and 2 mRNA in U‐937 cells

“…PGE2 can induce apoptosis in mononuclear cells in vitro as well as in vivo under various conditions [8,9,27,28], although it has also been reported to suppress activation-induced apoptosis [10]. In murine B-cell lines, a dose-dependent growth inhibition of immature cells was reported, whereas mature cell lines were less susceptible [20].…”