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Abstract
Background and aims. Carbonic anhydrases (CA) play a central role in osteoclast function and bone remodeling by catalyzing the formation of bicarbonate and proton from carbon dioxide. According to previous histochemical studies, advanced atherosclerotic plaques share similarities with bone. However, whether CAs are expressed in plaques is not known.
Methods and results. Whole genome expression array of arterial samples (n = 24) confirmed that several genes indicating osteoblastogenesis and osteoclastogenesis were up-regulated in plaques when compared to control vessel samples from internal thoracic arteries (n = 6), including CA2 and CA12, expression of which was also verified with quantitative reverse transcription polymerase chain reaction (RT-PCR). In atherosclerotic plaques there was 11.6-fold (P < 0.0001) and 11.4-fold (P < 0.0001) up-regulation of CA2 and CA12, compared to controls, respectively. According to quantitative PCR, CA2 expression was elevated in carotid (12.3-fold, P < 0.0001), femoral (13.2-fold, P < 0.01), and aortic plaques (7.5-fold, P < 0.0001). CA12 expression was elevated in carotid (11.6-fold, P < 0.0001), femoral (11.5-fold, P < 0.01), and aortic plaques (9.7-fold, P < 0.0001). CAII, CAXII, and CD68 and tartrate-resistant acid phosphatase (TRAP), a marker of osteoclast-like cells, were found to be co-localized in multinucleated giant cells in the atherosclerotic plaques using immunohistochemistry and double-staining immunofluorescence analysis.
Conclusions. The present findings provide evidence for the involvement of CAs in advanced atherosclerosis in osteoclast-like cells of monocyte-macrophage lineage.
Acknowledgements
The authors wish to thank Mrs Ulla Jukarainen, Nina Peltonen, Ms Elli Oksala, and Ms Rosanna Oksala for their skillful technical assistance.
Declaration of interest: This research is funded by European Union 7th Framework Program grant number 201668, Atheroremo. This study was supported with grants from the Medical Research Fund of Tampere University Hospital, the Emil Aaltonen Foundation (T.L.), the Pirkanmaa Regional Fund of the Finnish Cultural Foundation, the Research Foundation of Orion Corporation, the Jenny and Antti Wihuri Foundation, and the Academy of Finland (Grant no. 104821). Niku Oksala was supported by grants from the Finnish Angiology Association, Maire Taponen Foundation, and Paavo Nurmi Foundation. Niku Oksala and Mari Levula contributed equally to the work.