有哪些信誉好的足球投注网站a soluble factor from trypanosoma cruzi inhibits transforming growth factor-？-induced map kinase activation and gene expression in dermal fibroblasts鲁兹锥体的可溶性因子抑制转化生长因子- 全身的map激酶激活和真皮成纤维细胞的基因表达.pdfVIP
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a soluble factor from trypanosoma cruzi inhibits transforming growth factor-？-induced map kinase activation and gene expression in dermal fibroblasts鲁兹锥体的可溶性因子抑制转化生长因子- 全身的map激酶激活和真皮成纤维细胞的基因表达
A Soluble Factor from Trypanosoma cruzi Inhibits Transforming Growth Factor-ß-Induced MAP Kinase Activation and Gene Expression in Dermal Fibroblasts G. Adam Mott¤a, Jaime A. Costales¤b, Barbara A. Burleigh* Department of Immunology and Infectious Diseases, Harvard School of Public Health, Boston, Massachusetts, United States of America Abstract The protozoan parasite Trypanosoma cruzi, which causes human Chagas’ disease, exerts a variety of effects on host extracellular matrix (ECM) including proteolytic degradation of collagens and dampening of ECM gene expression. Exposure of primary human dermal fibroblasts to live infective T. cruzi trypomastigotes or their shed/secreted products results in a rapid down-regulation of the fibrogenic genes collagenIa1, fibronectin and connective tissue growth factor (CTGF/CCN2). Here we demonstrate the ability of a secreted/released T. cruzi factor to antagonize ctgf/ccn2 expression in dermal fibroblasts in response to TGF-ß, lysophosphatidic acid or serum, where agonist-induced phosphorylation of the mitogen- activated protein (MAP) kinases Erk1/2, p38 and JNK was also inhibited. Global analysis of gene expression in dermal fibroblasts identified a discrete subset of TGF-ß-inducible genes involved in cell proliferation, wound repair, and immune regulation that are inhibited by T. cruzi secreted/released factors, where the genes exhibiting the highest sensitivity to T. cruzi are known to be regulated by MAP kinase-activated transcription factors. Consistent with this observation, the Ets- family transcription factor binding site in the proximal promoter region of the ctgf/ccn2 gene ( 291 bp to 284 bp) was shown to be required for T. cruzi-mediated down-regulation of ctgf/ccn2 reporter expression. The cumulative data suggest a model in which T. cruzi
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