TY - JOUR
T1 - The human cytomegalovirus chemokine receptor US28 mediates vascular smooth muscle cell migration
AU - Streblow, Daniel N.
AU - Soderberg-Naucler, Cecilia
AU - Vieira, Jeffrey
AU - Smith, Patricia
AU - Wakabayashi, Eiko
AU - Ruchti, Franziska
AU - Mattison, Kirsten
AU - Altschuler, Yoram
AU - Nelson, Jay
N1 - Funding Information:
We thank Dr. David Johnson, Dr. Susan Orloff, Dr. David Kabat, Dr. Ashlee Moses, Dr. Gary Thomas, Dr. James Hicks, and Dr. Michael Jarvis for their helpful discussion. We are also grateful to Dr. David Johnson and Dr. Jessica Bonnam for their aid with the adenovirus construction techniques. We also thank Andrew Townsend for his graphical work. This work was supported in part by a Public Service Grant from the National Institutes of Health (AI 21640) (J. A. N.) and Activated Cell Systems, LLC (J. A. N.), and the Knut and Alice Wallenbergs Foundation (C. S.-N.). C. S.-N. is a scholar of the Wenner-Gren Foundation, Sweden. D. N. S. is supported by a National Research Service Award.
PY - 1999/11/24
Y1 - 1999/11/24
N2 - Human cytomegalovirus (HCMV) infection of smooth muscle cells (SMCs) in vivo has been linked to a viral etiology of vascular disease. In this report, we demonstrate that HCMV infection of primary arterial SMCs results in significant cellular migration. Ablation of the chemokine receptor, US28, abrogates SMC migration, which is rescued only by expression of the viral homolog and not a cellular G protein-coupled receptor (GPCR). Expression of US28 in the presence of CC chemokines including RANTES or MCP-1 was sufficient to promote SMC migration by both chemokinesis and chemotaxis, which was inhibited by protein tyrosine kinase inhibitors. US28-mediated SMC migration provides a molecular basis for the correlative evidence that links HCMV to the acceleration of vascular disease.
AB - Human cytomegalovirus (HCMV) infection of smooth muscle cells (SMCs) in vivo has been linked to a viral etiology of vascular disease. In this report, we demonstrate that HCMV infection of primary arterial SMCs results in significant cellular migration. Ablation of the chemokine receptor, US28, abrogates SMC migration, which is rescued only by expression of the viral homolog and not a cellular G protein-coupled receptor (GPCR). Expression of US28 in the presence of CC chemokines including RANTES or MCP-1 was sufficient to promote SMC migration by both chemokinesis and chemotaxis, which was inhibited by protein tyrosine kinase inhibitors. US28-mediated SMC migration provides a molecular basis for the correlative evidence that links HCMV to the acceleration of vascular disease.
UR - http://www.scopus.com/inward/record.url?scp=0033601104&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0033601104&partnerID=8YFLogxK
U2 - 10.1016/S0092-8674(00)81539-1
DO - 10.1016/S0092-8674(00)81539-1
M3 - Article
C2 - 10589679
AN - SCOPUS:0033601104
SN - 0092-8674
VL - 99
SP - 511
EP - 520
JO - Cell
JF - Cell
IS - 5
ER -