期刊
JOURNAL OF EUKARYOTIC MICROBIOLOGY
卷 49, 期 5, 页码 383-390出版社
SOC PROTOZOOLOGISTS
DOI: 10.1111/j.1550-7408.2002.tb00216.x
关键词
Chagas' disease; EGF receptors; kinase activity; ligand-receptor binding; MAP kinase; Northern blot; protein kinase C; receptor-mediated endocytosis; Scatchard Plot; trypanosome growth
类别
资金
- NCRR NIH HHS [RR 03032] Funding Source: Medline
- NHLBI NIH HHS [HL 03156] Funding Source: Medline
Host growth factors induce proliferation of Trypanosoma cruzi amastigotes by mechanisms that remain poorly defined. Here we examined human epidermal growth factor (EGF) for its ability to bind to the mammalian multiplicative forms of T. cruzi and to induce growth of the parasites. EGF stimulated incorporation of [H-3] thymidine into DNA and growth of amastigotes both in a concentration-dependent manner. Radiolabeled EGF was found to bind to amastigotes in a concentration-dependent and saturable manner but it did not bind to trypomastigotes. Scatchard analysis showed a single class of receptors with a K-d of 0.8 nM and numbering 3.1 X 103 per amastigote. Results from internalization experiments provided evidence of receptor-mediated endocytosis of EGF. Northern analysis showed a 3.0-kb transcript for the putative EGF receptor (EGFR) homologue in amastigotes, but not trypomastigotes. Binding of EGF to amastigotes induced signal transduction events. EGF induced in vitro kinase activity as determined by gamma-[P-32] ATP incorporation into amastigote proteins. EGF also increased protein kinase C activity in a concentration-dependent manner and Mitogen Activated Protein (MAP) kinase activity in a time- and concentration-dependent manner. A specific inhibitor (AG14782) of the EGFR and a MAP kinase inhibitor (PD98059) decreased EGF-dependent T. cruzi MAP kinase activity. These results describe a novel mechanism used by amastigotes to regulate their proliferation mediated by an EGF-dependent signal transduction pathway.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据