Open AccessDown-regulation of integrin 1/beta1 expression and association with cell rounding in human cytomegalovirus-infected fibroblasts
Author(s) -
Andrew P. Warren,
C. N. Owens,
L. K. Borysiewicz,
Kishan Patel
Publication year - 1994
Publication title -
journal of general virology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.55
H-Index - 167
eISSN - 1465-2099
pISSN - 0022-1317
DOI - 10.1099/0022-1317-75-12-3319
Subject(s) - integrin , biology , laminin , human cytomegalovirus , integrin alpha m , microbiology and biotechnology , cell , cell adhesion , immunoprecipitation , alpha (finance) , collagen receptor , beta (programming language) , extracellular matrix , cell culture , virology , virus , biochemistry , medicine , genetics , construct validity , nursing , computer science , patient satisfaction , programming language
Human cytomegalovirus (HCMV) causes a c.p.e. characterized by rounding of the infected cell. Since interactions with the extracellular matrix may be involved in the cell rounding, we have analysed the expression of integrins, which are the main cell surface receptors involved in cell-substrate adhesion and spreading. By FACS analysis, a selective decrease in cell surface expression of alpha 1/beta 1 integrin was observed in HCMV-infected fibroblasts. This decrease coincides with cell rounding. Immunoprecipitation studies and FACS analysis of permeabilized cells have further demonstrated that total levels of this integrin are decreased in infected cells, suggesting that the reduction in cell surface alpha 1/beta 1 integrin is not due to a defect in transport to the surface. Furthermore, we have ruled out the possibility that the observed decrease in alpha 1/beta 1 expression is caused by a cytokine released from the infected cells by showing that the reduction is abolished by inactivating the HCMV with u.v. irradiation, and that conditioned medium from HCMV-infected cells has no effect on expression of alpha 1/beta 1 integrin in uninfected cells. Concomitant with the reduction in alpha 1/beta 1 levels, the HCMV-infected fibroblasts show a reduced ability to adhere to laminin and collagen IV. Taken together the data indicate that de novo synthesis of HCMV protein(s) causes a decreased assembly/expression of alpha 1/beta 1 integrin, coincident with the well characterized morphological alterations of the infected cell.