Journal
HUMAN IMMUNOLOGY
Volume 72, Issue 12, Pages 1150-1159Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.humimm.2011.09.004
Keywords
Anti-HLA antibodies; Human smooth muscle cells; Focal adhesion kinase; Cell migration; Cell proliferation
Categories
Funding
- American Heart Association
- National Institute of Allergy and Infectious Diseases [RO1 AI 042819]
- National Institutes of Health [U01AI077821]
- National Heart, Lung and Blood Institute [RO1 HL 090995]
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Chronic rejection manifests as transplant vasculopathy, which is characterized by intimal thickening of the vessels of the allograft. Intimal thickening is thought to result from the migration and proliferation of vascular smooth muscle cells (SMC) in the vessel media, followed by deposition of extracellular matrix proteins. The development of post-transplantation anti- human leukocyte antigen (HLA) antibodies (Ab) is strongly correlated with the development of transplant vasculopathy and graft loss. Here we demonstrate that cross-linking of HLA class I molecules on the surface of human SMC with anti-HLA class I Ab induced cell proliferation and migration. Class I ligation also increased phosphorylation of focal adhesion kinase (FAK), Akt, and ERK1/2 in SMC. Knockdown of FAK by siRNA attenuated class I-induced phosphorylation of Akt and ERK1/2, as well as cell proliferation and migration. These results indicate that ligation of HLA class I molecules induces SMC migration and proliferation in a FAK-dependent manner, which may be important in promoting transplant vasculopathy. (C) 2011 American Society for Histocompatibility and Immunogenetics. Published by Elsevier Inc. All rights reserved.
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