Evidence that protease activated receptor 2 expression is enhanced in human coronary atherosclerotic lesions

C. Napoli, F. De Nigris, J. L. Wallace, M. D. Hollenberg, G. Tajana, G. De Rosa, V. Sica, G. Cirino

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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.

Original languageEnglish
Pages (from-to)513-516
Number of pages4
JournalJournal of Clinical Pathology
Volume57
Issue number5
DOIs
Publication statusPublished - May 2004

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PAR-2 Receptor
Monoclonal Antibodies
Blood Vessels
Epitopes
Foam Cells
Antibodies
Vascular System Injuries
Malondialdehyde
Lysine
Coronary Vessels
Arteries
Macrophages
Pharmacology
Rabbits

ASJC Scopus subject areas

  • Pathology and Forensic Medicine

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Evidence that protease activated receptor 2 expression is enhanced in human coronary atherosclerotic lesions. / Napoli, C.; De Nigris, F.; Wallace, J. L.; Hollenberg, M. D.; Tajana, G.; De Rosa, G.; Sica, V.; Cirino, G.

In: Journal of Clinical Pathology, Vol. 57, No. 5, 05.2004, p. 513-516.

Research output: Contribution to journalArticle

Napoli, C, De Nigris, F, Wallace, JL, Hollenberg, MD, Tajana, G, De Rosa, G, Sica, V & Cirino, G 2004, 'Evidence that protease activated receptor 2 expression is enhanced in human coronary atherosclerotic lesions', Journal of Clinical Pathology, vol. 57, no. 5, pp. 513-516. https://doi.org/10.1136/jcp.2003.015156
Napoli, C. ; De Nigris, F. ; Wallace, J. L. ; Hollenberg, M. D. ; Tajana, G. ; De Rosa, G. ; Sica, V. ; Cirino, G. / Evidence that protease activated receptor 2 expression is enhanced in human coronary atherosclerotic lesions. In: Journal of Clinical Pathology. 2004 ; Vol. 57, No. 5. pp. 513-516.
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AU - Napoli, C.

AU - De Nigris, F.

AU - Wallace, J. L.

AU - Hollenberg, M. D.

AU - Tajana, G.

AU - De Rosa, G.

AU - Sica, V.

AU - Cirino, G.

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N2 - 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.

AB - 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.

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