Evidence that protease activated receptor 2 expression is enhanced in human coronary atherosclerotic lesions
- 1Department of Clinical Pathology and Medicine, University of Naples, Naples, 80128 Italy
- 2Department of Pharmacological Sciences, University of Salerno, Salerno, 84084 Italy
- 3Department of Human Pathology, University of Naples, 80131 Italy
- 4Department of Pharmacology and Therapeutics, University of Calgary, Alberta, T2N 4N1 Canada
- 5Department of Experimental Pharmacology, University of Naples, 80131 Italy
- Correspondence to: Dr C Napoli Department of Clinical Pathology and Medicine, University of Naples, PO Box 80128, Naples, Italy; claunaptin.it
- Accepted 26 January 2004
Abstract
Aim: To investigate protease activated receptor 2 (PAR-2) expression in human coronary atherosclerotic lesions because PAR-2 is involved in the modulation of inflammatory events and vascular function.
Methods: An immunohistochemical analysis was performed on serial arterial sections, using the following antibodies: MDA2, a murine monoclonal antibody against malondialdehyde lysine epitopes of oxidised low density lipoprotein (oxLDL); HAM-56, a monoclonal antibody against human macrophages/foam cells; B5, a rabbit polyclonal antibody against PAR-2; and SAM11, a mouse monoclonal antibody against human PAR-2. Sections containing at least one lesion showing substantial immunostaining were counted as positive, and results were expressed as per cent of all sections of the same artery.
Results: PAR-2 expression was enhanced in human coronary atherosclerotic lesions. This phenomenon correlated with an increase in oxLDL epitopes in the coronary artery.
Conclusion: This study shows for the first time that PAR-2 expression is enhanced in human coronary atherosclerotic lesions, and suggests that PAR-2 dependent cellular trafficking may be one of the regulatory signalling responses to vascular injury. Further pharmacological studies will establish whether modulation (and in which direction) of PAR-2 represents a possible therapeutic target for controlling the vascular response to injury.
- oxLDL, oxidised low density lipoprotein
- PAR-2, protease activated receptor 2
- PBS, phosphate buffered saline









