Skip to main content
Figure 5 | Journal of Neuroinflammation

Figure 5

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 5

Matrix metalloproteinase (MMP)-3 promoter activity. (A) Schematic representation of full-length MMP-3 promoter demonstrating relevant promoter binding sites (shaded boxes). Right to left arrow represents transcription start site. Left to right arrows represent transcription stopping sites on the three promoter constructs, for which the length is indicated by the black line below. Of note, the 1612 bp construct disrupts a stromelysin IL-1 responsive element (SIRE) binding site. (B) MMP-3 promoter deletion constructs. Microglial cells were transiently transfected with full-length promoter (black bars) or deletion constructs (gray bars), and stimulated with, conditioned media from control monocytes (CoMCont) or conditioned media from tuberculosis (TB)-infected monocytes (CoMTb) for 24 hours. CoMTb-stimulated full-length MMP-3 promoter was designated as maximal luciferase activity (100%), and other results are expressed as a percentage of this maximum. Bars are mean ± SD from three samples and represent at least three separate experiments performed in triplicate. Data were analyzed by the Student t-test (** P <0.01).

Back to article page

Journal of Neuroinflammation

ISSN: 1742-2094