A simplified overview of the LPS-induced NF-κB signalling pathway.

<p>IκB, nuclear factor of kappa light polypeptide gene enhancer in B-cells inhibitor (alpha, beta and epsilon isoforms are incorporated into the model); IKK, IκB kinase; LPS, lipopolysaccharide; MyD88, myeloid differentiation primary response gene 88; NF-κB, nuclear factor kappa B; TLR4, toll-like receptor 4; TNFα, tumour necrosis factor alpha; TNFR, tumour necrosis factor receptor; TRIF, Tir-Domain-Containing Adapter-Inducing Interferon-β.</p

NF-κB time course behaviour in TRIF and MyD88 knock-out conditions.

<p>A. Concentrations of nuclear NF-κB over time, simulated using TRIF and MyD88 knock-out versions of the <i>in silico</i> model described here, B. Concentrations of nuclear NF-κB over time, simulated using TRIF and MyD88 knock-out versions of the <i>in silico</i> model described by Covert et al., C. Experimental <i>in vitro</i> data from LPS-treated TRIF or MyD88 knock-out mouse embryo fibroblasts as described by Covert et al. <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0070180#pone.0070180-Covert1" target="_blank">[22]</a>. B and C are reprinted from Covert, M. W., Leung, T. H., Gaston, J. E., & Baltimore, D. (2005). Achieving stability of lipopolysaccharide-induced NF-kappaB activation. <i>Science (New York, N.Y.)</i>, <i>309</i>(5742), 1854-7. under a CC BY license, with permission from AAAS, original copyright 2005.</p

Steady state concentrations at different doses of LPS.

<p>A. <i>In silico</i> simulation of steady state concentrations of inactive and phosphorylated IKK, and B. <i>In silico</i> simulation of steady state concentrations of free nuclear and cytoplasmic NF-κB.</p

IKK time course behaviour.

<p>A. Concentrations of nuclear IKK over time, simulated using the <i>in silico</i> model described here, B. Experimental data from LPS-treated mouse embryo fibroblasts as described by Covert et al. <a href="http://www.plosone.org/article/info:doi/10.1371/journal.pone.0070180#pone.0070180-Covert1" target="_blank">[22]</a>. B is reprinted from Covert, M. W., Leung, T. H., Gaston, J. E., & Baltimore, D. (2005). Achieving stability of lipopolysaccharide-induced NF-kappaB activation. <i>Science (New York, N.Y.)</i>, <i>309</i>(5742), 1854-7. under a CC BY license, with permission from AAAS, original copyright 2005.</p

NF-κB time course behaviour of A. Concentrations of nuclear NF-κB over time, simulated using the <i>in silico</i> model described here, B. Concentrations of nuclear NF-κB over time, simulated using the <i>in silico</i> model described by Covert et al., C. Experimental data from LPS-treated mouse embryo fibroblasts as described by Covert et al. [22].

<p>C is reprinted from Covert, M. W., Leung, T. H., Gaston, J. E., & Baltimore, D. (2005). Achieving stability of lipopolysaccharide-induced NF-kappaB activation. <i>Science (New York, N.Y.)</i>, <i>309</i>(5742), 1854-7. under a CC BY license, with permission from AAAS, original copyright 2005.</p

TGF-β1, TGF-βR1, TGF-βR2, and pSmad 2/3, are localized to the mesothelial cells of the peritoneum of women without endometriosis at contol sites and prone sites.

<p>TGF-β1, TGF-βR1, TGF-βR2, and pSmad 2/3, are localized to the mesothelial cells of the peritoneum of with endometriosis at sites disteal and ajacent to endometriosis lesions. No staining was observed in the negative control sections. <i>n = 8.</i></p

Table displays gene expression including fold change and p value of TGF-β signalling target genes in peritoneal biopsies from women with endometriosis at sites ajacent compared to sites distal to endometriosis lesions.

<p><i>n = 6.</i></p><p>Table displays gene expression including fold change and p value of TGF-β signalling target genes in peritoneal biopsies from women with endometriosis at sites ajacent compared to sites distal to endometriosis lesions.</p

<i>TGFB1</i> mRNA expression was significantly increased in the peritoneum adjacent to endometriosis lesions compared to peritoneum distal to lesions in women with endometriosis (B).

<p>There was no signifianct difference in TGFB1 expression between women with and without endometriosis, nor was there a difference in expression between control and prone sites of peritoneum in women without endometriosis. There is no significant change in mRNA expression for <i>TGFBR1, TGFBR2</i> and <i>SMAD3</i> in all comparisons made (A, C–L). <i>n = 35 (*p<0.05).</i></p

All TGF-β ligands are expressed in peritoneal fluid from women with and without endometriosis.

<p>TGF-β1 was significantly increased in peritoneal fluid from women with endometriosis compared to women without. Levels of TGF-β2 do not change between women with and without endometriosis. TGF-β3 levels appear to increase in women with endometriosis however this is not a significant change. Cultured HPMCs secreted TGF-β1 protein in-vitro. <i>n = 12 peritoneal fluid, n = 3 HMPC (*p<0.05).</i></p

Primers used for qRT-PCR including primer sequence.

<p>All primers were pre-validated and supplied by Primer Design.</p><p>Primers used for qRT-PCR including primer sequence.</p