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Figure 2 | Journal of Neuroinflammation

Figure 2

From: In an in vitro model of human tuberculosis, monocyte-microglial networks regulate matrix metalloproteinase-1 and -3 gene expression and secretion via a p38 mitogen activated protein kinase-dependent pathway

Figure 2

Conditioned media from tuberculosis (TB)-infected monocytes (CoMTb) drive phosphorylation of the extracellular signal-regulated kinase (ERK), p38 and AKT mitogen-activated protein kinase (MAPK) pathways in microglial cells. (A) Proteome profiler array of conditioned media from control monocytes (CoMCont)- and CoMTb-stimulated microglia at 30 minutes. CoMTb drives p38 activity and further phosphorylation of constitutive ERK 1/2 and AKT activity. (B) Densitometric analysis of phospho-array. Densitometric analysis of differences in mean spot intensity between CoMCont- and CoMTb-stimulated cells is presented, demonstrating that the p38α and p38γ subunits are the principal CoMTb up-regulated MAP kinases. (C) p38 phosphorylation kinetics. CoMTb drives up-regulation of p38 at 15 minutes, with a second peak at 120 minutes. (D) CoMCont-stimulated microglial ERK activity at 30 minutes shows high basal activity further up-regulated by CoMTb. Only CoMTb activity was blocked by the inhibitor PD98059. Representative data from three independent experiments are shown. Bars represent mean +/− standard error of the mean from three independent experiments. * P <0.05, ** P <0.01.

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Journal of Neuroinflammation

ISSN: 1742-2094