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Am J Physiol Cell Physiol 282: C538-C544, 2002. First published November 7, 2001; doi:10.1152/ajpcell.00419.2001
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Vol. 282, Issue 3, C538-C544, March 2002

Adenoviral gene transfer of PDGF downregulates gas gene product PDGFalpha R and prolongs ERK and Akt/PKB activation

Qi-Ping Chen and William V. Giannobile

Center for Biorestoration of Oral Health and Department of Periodontics, Prevention and Geriatrics, University of Michigan, Ann Arbor, Michigan 48109-1078

The delivery of platelet-derived growth factor (PDGF) for tissue engineering of skin and periodontal wounds has become an active area of interest. However, little is known regarding the extended effects of PDGF on cell signaling via gene therapy and how such an approach facilitates the exiting of cells from growth arrest and entry to competence required for cell cycling. We show in vitro expression and secretion of PDGF-AA by recombinant adenovirus encoding the PDGF-A gene (Ad-PDGF-A). The bioactive PDGF-AA protein released induces sustained downregulation of PDGFalpha R that is encoded by a growth arrest-specific (gas) gene. Ad-PDGF-A induces sustained phosphorylation of PDGFalpha R as well as prolonged phosphorylation of downstream extracellular signal-regulated kinase 1/2 and Akt signaling pathways. Furthermore, the phosphorylation of PDGFalpha R is abolished by cotransducing cells with adenovirus encoding a dominant negative mutant of the PDGF-A gene that disrupts PDGF bioactivity. These findings demonstrate the prolonged effects of adenoviral delivery of PDGF and aid in the better understanding of sustained PDGF signaling.

platelet-derived growth factor; growth arrest; extracellular signal-regulated kinase; Akt/protein kinase B


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