ABSTRACT
Murine macrophages of the J774A.1 line are hydrogen sulphide-producing cells with the primary role of γ-cystathionase (CTH) and secondary role of 3-mercaptopyruvate sulfurtransferase (limited by cysteine availability) and with a negligible role of cystathionine ß-synthase (CBS) in H2S generation. J774A.1 cells stimulation with lipopolysaccharide (LPS) or interferon-gamma (IFNγ) resulted in decreased H2S levels after 24 h of incubation; however, they were restored to the control level after 48 h. Negligible CBS expression and activity in J774A.1 cells can result in homocysteine availability for CTH-catalyzed, H2S-generating reactions. This was supported by an increased CTH expression (IFNγ, 24 h and 48 h, and LPS, 48 h) and activity (24 h, LPS) in the stimulated cells. The results confirm the suggested feedback regulation between CBS and CTH.
Subject(s)
Hydrogen Sulfide/metabolism , Interferon-gamma/pharmacology , Lipopolysaccharides/pharmacology , Macrophages/metabolism , Animals , Cell Line , Cystathionine beta-Synthase/metabolism , Cystathionine gamma-Lyase/biosynthesis , Cystathionine gamma-Lyase/metabolism , Cysteine/metabolism , Homocysteine/metabolism , Macrophages/drug effects , Mice , Mice, Inbred BALB C , Sulfurtransferases/biosynthesis , Sulfurtransferases/metabolismABSTRACT
We have previously reported that the blockage of TrkB and TrkC signaling in primary culture of opossum neocortical cells affects neurogenesis that involves a range of processes including cell proliferation, differentiation, and survival. Here, we studied whether TrkB and TrkC activity specifically affects various types of progenitor cell populations during neocortex formation in the Monodelphis opossum in vivo. We found that the inhibition of TrkB and TrkC activities affects the same proliferative cellular phenotype, but TrkC causes more pronounced changes in the rate of cell divisions. Additionally, inhibition of TrkB and TrkC does not affect apoptosis in vivo, which was found in cell culture experiments. The lack of TrkB and TrkC receptor activity caused the arrest of newly generated neurons; therefore, they could not penetrate the subplate zone. We suggest that at this time point in development, migration consists of 2 steps. During the initial step, neurons migrate and reach the base of the subplate, whereas during the next step the migration of neurons to their final position is regulated by TrkB or TrkC signaling.