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Gene network analysis during early infection of human coronary artery smooth muscle cells by Trypanosoma cruzi and its gp83 ligand
Author(s) -
Johnson Candice Angella,
Nde Pius,
Pratap Siddharth,
Cardenas Tatiana C,
Kleshchenko Yulia,
Furtak Vyachslav A,
Lima Maria F,
Villalta Fernando
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.671.1
Subject(s) - trypanosoma cruzi , biology , interactome , gene silencing , chagas disease , transcriptome , gene , wrky protein domain , gene expression , microbiology and biotechnology , immunology , genetics , world wide web , computer science , parasite hosting
Trypanosoma cruzi, the causative agent of Chagas disease, infects heart and muscle cells leading to cardiac arrest followed by death. The genetic architectures in the early T. cruzi infection process of human cells are unknown. To understand the genetic architectures of the early invasion process of T. cruzi, we conducted gene transcription microarray analysis followed by gene network construction of the host cell response in human coronary artery smooth muscle primary cells (HCASMC) infected with T. cruzi or exposed to T. cruzi gp83, a ligand used by the trypanosome to bind host cells. Using seven RT‐PCR verified up‐regulated genes (FOSB, ATF5, INPP1, CCND2, THBS1, LAMC1, and APLP2) as the seed for network construction, we built an interaction network of early T. cruzi infection process containing 165 genes, connected by 598 biological interactions. This interactome network is centered on the BCL6 gene as a hub. Silencing the expression of two seed genes (THBS1 and LAMC1) by RNAi reduced T. cruzi infection. Overall, our results elucidate the significant and complex process involved in T. cruzi infection of HCASMC at the transcriptome level. This is the first elucidation into the interactome network in human cells caused by T. cruzi and its gp83 ligand (Supported by NIH grants AI080580‐03 and AI007281‐21).