首页> 外文期刊>International journal of medical microbiology: IJMM >Bacteria induce CTGF and CYR61 expression in epithelial cells in a lysophosphatidic acid receptor-dependent manner
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Bacteria induce CTGF and CYR61 expression in epithelial cells in a lysophosphatidic acid receptor-dependent manner

机译:细菌以溶血磷脂酸受体依赖性方式诱导上皮细胞中CTGF和CYR61的表达

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Cysteine-rich protein 61 (Cyr61/CCN1) and connective tissue growth factor (CTGF/CCN2) are members of the CCN (CYR61, CTGF, nephroblastoma overexpressed gene) family and exert pleiotropic functions such as regulation of adhesion, migration, extracellular matrix deposition, or cell differentiation, and play an important role in wound healing. This study focused on the nature of the so far unknown CTGF and CYR61 mRNA expression of epithelial cells after infection with bacteria. We demonstrate that infection of epithelial cells with attenuated Yersinia enterocolitica lacking the virulence plasmid pYV leads to the expression of CYR61 and CTGF. Virulent Y. enterocolitica bearing the pYV virulence plasmid suppressed the mRNA expression of these genes. Yersinia-mediated inhibition of CTGF and CYR61 mRNA expression is partially mediated by the cysteine protease YopT. Further characterization of the Yersinia factors, which trigger CTGF and CYR61 mRNA expression, demonstrated that these factors were secreted and could be enriched in lipid extracts. Beside Yersinia, several other bacteria such as Escherichia coli, Pseudomonas aeruginosa, Enterococcus faecalis, or Staphylococcus aureus, as well as supernatants of these bacteria induced CTGF and CYR61 expression. Blocking experiments with the lysophosphatidic acid (LPA) receptor-specific inhibitor Kil6425 suggest a general involvement of LPA receptors in bacteria-triggered CTGF and CYR61 expression. These data suggest that LPA receptor-dependent expression of CTGF and CYR61 represents a common host response after interaction with bacteria. (c) 2007 Elsevier GmbH. All rights reserved.
机译:富含半胱氨酸的蛋白61(Cyr61 / CCN1)和结缔组织生长因子(CTGF / CCN2)是CCN(CYR61,CTGF,肾母细胞瘤过表达的基因)家族的成员,并发挥多效性功能,例如调节粘附,迁移,细胞外基质沉积或细胞分化,并在伤口愈合中起重要作用。这项研究的重点是细菌感染后上皮细胞迄今未知的CTGF和CYR61 mRNA表达的性质。我们证明缺乏毒性质粒pYV的减毒小肠结肠炎耶尔森氏菌感染上皮细胞导致CYR61和CTGF的表达。携带pYV毒力质粒的强毒小肠结肠炎耶尔森氏菌抑制了这些基因的mRNA表达。耶尔森氏菌介导的CTGF和CYR61 mRNA表达抑制部分由半胱氨酸蛋白酶YopT介导。触发CTGF和CYR61 mRNA表达的耶尔森氏菌因子的进一步表征表明,这些因子是分泌的,可以在脂质提取物中富集。除耶尔森氏菌外,其他几种细菌,例如大肠杆菌,铜绿假单胞菌,粪肠球菌或金黄色葡萄球菌,以及这些细菌的上清液均诱导CTGF和CYR61表达。用溶血磷脂酸(LPA)受体特异性抑制剂Kil6425进行的阻断实验表明,LPA受体普遍参与细菌触发的CTGF和CYR61表达。这些数据表明,与细菌相互作用后,CTPA和CYR61的LPA受体依赖性表达代表了常见的宿主反应。 (c)2007 Elsevier GmbH。版权所有。

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