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Original article
Evidence that protease activated receptor 2 expression is enhanced in human coronary atherosclerotic lesions
  1. C Napoli1,
  2. F de Nigris2,
  3. J L Wallace4,
  4. M D Hollenberg4,
  5. G Tajana2,
  6. G De Rosa3,
  7. V Sica1,
  8. G Cirino5
  1. 1Department of Clinical Pathology and Medicine, University of Naples, Naples, 80128 Italy
  2. 2Department of Pharmacological Sciences, University of Salerno, Salerno, 84084 Italy
  3. 3Department of Human Pathology, University of Naples, 80131 Italy
  4. 4Department of Pharmacology and Therapeutics, University of Calgary, Alberta, T2N 4N1 Canada
  5. 5Department of Experimental Pharmacology, University of Naples, 80131 Italy
  1. Correspondence to:
 Dr C Napoli
 Department of Clinical Pathology and Medicine, University of Naples, PO Box 80128, Naples, Italy; claunaptin.it

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
  • atherosclerosis
  • protease activated receptor 2
  • inflammation

https://doi.org/10.1136/jcp.2003.015156

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