title: Microarray profiling analysis uncovers common molecular mechanisms of rubella virus, human cytomegalovirus, and herpes simplex virus type 2 infections in ECV304 cells.
abstract: To study the common molecular mechanisms of various viruses infections that might result in congential cardiovascular diseases in perinatal period, changes in mRNA expression levels of ECV304 cells infected by rubella virus (RUBV), human cytomegalovirus (HCMV), and herpes simplex virus type 2 (HSV-2) were analyzed using a microarray system representing 18,716 human genes. 99 genes were found to exhibit differential expression (80 up-regulated and 19 down-regulated). Biological process analysis showed that 33 signaling pathways including 22 genes were relevant significantly to RV, HCMV and HSV-II infections. Of these 33 biological processes, 28 belong to one-gene biological processes and 5 belong to multiple-gene biological processes. Gene annotation indicated that the 5 multiple-gene biological processes including regulation of cell growth, collagen fibril organization, mRNA transport, cell adhesion and regulation of cell shape, and seven down- or up-regulated genes [CRIM1 (cysteine rich transmembrane BMP regulator 1), WISP2 (WNT1 inducible signaling pathway protein 2), COL12A1 (collagen, type XII, alpha 1), COL11A2 (collagen, type XI, alpha 2), CNTN5 (contactin 5), DDR1 (discoidin domain receptor tyrosine kinase 1), VEGF (vascular endothelial growth factor precursor)], are significantly correlated to RUBV, HCMV and HSV-2 infections in ECV304 cells. The results obtained in this study suggested the common molecular mechanisms of viruses infections that might result in congential cardiovascular diseases.
authors.affiliation: The Center for Heart Development, Key Lab of National Education Ministry, College of Life Sciences, Hunan Normal University, Changsha, Hunan China. moxiaoyang@yahoo.com.cn
authors.forename: X
authors.initials: X
authors.lastname: Mo
authors.forename: L
authors.initials: L
authors.lastname: Xu
authors.forename: Q
authors.initials: Q
authors.lastname: Yang
authors.forename: H
authors.initials: H
authors.lastname: Feng
authors.forename: J
authors.initials: J
authors.lastname: Peng
authors.forename: Y
authors.initials: Y
authors.lastname: Zhang
authors.forename: W
authors.initials: W
authors.lastname: Yuan
authors.forename: Y
authors.initials: Y
authors.lastname: Wang
authors.forename: Y
authors.initials: Y
authors.lastname: Li
authors.forename: Y
authors.initials: Y
authors.lastname: Deng
authors.forename: Y
authors.initials: Y
authors.lastname: Wan
authors.forename: Z
authors.initials: Z
authors.lastname: Chen
authors.forename: F
authors.initials: F
authors.lastname: Li
authors.forename: X
authors.initials: X
authors.lastname: Wu
mesh_terms: D002448:Cell Adhesion / Q000235:genetics; D002460:Cell Line; D002465:Cell Movement / Q000235:genetics; D049109:Cell Proliferation; D048430:Cell Shape / Q000235:genetics; D003094:Collagen / Q000378:metabolism; D003587:Cytomegalovirus / Q000235:genetics / Q000378:metabolism; D003586:Cytomegalovirus Infections / Q000235:genetics* / Q000821:virology; D015536:Down-Regulation; D020869:Gene Expression Profiling; D015967:Gene Expression Regulation, Viral; D006561:Herpes Simplex / Q000235:genetics* / Q000821:virology; D018258:Herpesvirus 2, Human / Q000235:genetics / Q000378:metabolism; D061307:Human Umbilical Vein Endothelial Cells / Q000821:virology; D006801:Humans; D046228:Microarray Analysis; D012333:RNA, Messenger / Q000378:metabolism; D012409:Rubella / Q000235:genetics* / Q000821:virology; D012412:Rubella virus / Q000235:genetics / Q000378:metabolism; D015398:Signal Transduction; D015854:Up-Regulation
chemical_list: D012333:RNA, Messenger; D003094:Collagen