Korean J Vasc Endovasc Surg.
2011 May;27(2):61-65. 10.5758/kjves.2011.27.2.61.
Role of Protein Kinase C-delta in Atherosclerosis
- Affiliations
-
- 1Department of Surgery, Ulsan University Hospital, University of Ulsan College of Medicine, Ulsan, Korea. hrcho@uuh.ulsan.kr
- 2Department of Thoracic Surgery, Ulsan University Hospital, University of Ulsan College of Medicine, Ulsan, Korea.
- 3School of Biological Sciences, University of Ulsan, Ulsan, Korea.
- 4Division of Vascular Surgery, Department of Surgery, Asan Medical Center, University of Ulsan College of Medicine, Seoul, Korea.
- KMID: 1448081
- DOI: http://doi.org/10.5758/kjves.2011.27.2.61
Abstract
- PURPOSE
Protein kinase C (PKC) has been implicated in a wide variety of cellular processes. Although PKC-delta is implicated in cell growth inhibition, as well as in cell differentiation, apoptosis, and tumor suppression, its role in atherosclerosis remains unclear. This study aimed to identify the mechanism of PKC-delta in the development of atherosclerosis.
METHODS
To induce atherosclerosis, we performed allograft transplantations on aortas in mice. At 2, 4, and 6 weeks after transplantation, grafted aortas were obtained to compare the degree of atherosclerosis between wild type and PKC-delta (-/-) aorta. Alloantibody levels in the recipient mice's blood were measured. Reverse transcriptase-polymerase chain reaction (RT-PCR) was performed to quantitatively measure chemokine and cytokine mRNA expression of the inflammation from the harvested aorta.
RESULTS
Atherosclerosis was more severe in the PKC-delta (-/-) aorta than in the wild type aorta. Alloantibody levels were higher in the mice grafted with aorta from the PKC-delta (-/-) mice than in the mice grafted with aorta from the wild type mice. RT-PCR revealed higher expressions of MRP-2, MCP-1, MIP-1alpha, and IL-2 in the mice grafted with aorta from the PKC-delta (-/-) mice than the wild type mice.
CONCLUSION
Aorta allograft transplantation is a useful modality for inducing atherosclerosis. PKC-delta may be a negative regulator of atherosclerosis.
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