Hartman Institute for Therapeutic Organ Regeneration

Induction of endogenous genes following infection of human endothelial cells with an E1(-) E4(+) adenovirus gene transfer vector.

TitleInduction of endogenous genes following infection of human endothelial cells with an E1(-) E4(+) adenovirus gene transfer vector.
Publication TypeJournal Article
Year of Publication1999
AuthorsRamalingam R, Rafii S, Worgall S, Hackett NR, Crystal RG
JournalJ Virol
Volume73
Issue12
Pagination10183-90
Date Published1999 Dec
ISSN0022-538X
KeywordsAdenovirus E1 Proteins, Adenovirus E4 Proteins, Adenoviruses, Human, Capsid, Cells, Cultured, DNA, Complementary, Endothelium, Vascular, Gene Deletion, Gene Expression Regulation, Viral, Gene Transfer Techniques, Genetic Vectors, Humans, Kinetics
Abstract

Recombinant adenovirus (Ad) gene transfer vectors are effective at transferring exogenous genes to a variety of cells and tissue types both in vitro and in vivo. However, in the process of gene transfer, the Ad vectors induce the expression of target cell genes, some of which may modify the function of the target cell and/or alter the local milieu. To develop a broader understanding of Ad vector-mediated induction of endogenous gene expression, genes induced by first-generation E1(-) E4(+) Ad vectors in primary human umbilical vein endothelial cells were identified by cDNA subtraction cloning. The identified cDNAs included signaling molecules (lymphoid blast crisis [LBC], guanine nucleotide binding protein alpha type S [Galpha-S], and mitogen kinase [MEK5]), calcium-regulated/cytoskeletal proteins (calpactin p11 and p36 subunits, vinculin, and spinocerebellar ataxia [SCA1]), growth factors (insulin-like growth factor binding protein 4 and transforming growth factor beta2), glyceraldehyde-6-phosphate dehydrogenase, an expressed sequence tag, and a novel cDNA showing homology to a LIM domain sequence. Two- to sevenfold induction of the endogenous gene expression was observed at 24 h postinfection, and induction continued up to 72 h, although the timing of gene expression varied among the identified genes. In contrast to that observed in endothelial cells, the Ad vector-mediated induction of gene expression was not found following Ad vector infection of primary human dermal fibroblasts or human alveolar macrophages. Empty Ad capsids did not induce endogenous gene expression in endothelial cells. Interestingly, additional deletion of the E4 gene obviated the upregulation of genes in endothelial cells by the E1(-) E3(-) Ad vector, suggesting that genes carried by the E4 region play a central role in modifying target cell gene expression. These findings are consistent with the notion that efficient transfer of exogenous genes to endothelial cells by first-generation Ad vectors comes with the price that these vectors also induce the expression of a variety of cellular genes.

DOI10.1128/JVI.73.12.10183-10190.1999
Alternate JournalJ Virol
PubMed ID10559334
PubMed Central IDPMC113071
Grant ListR01 HL 57318 / HL / NHLBI NIH HHS / United States

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