Bone morphogenetic protein expression in human atherosclerotic lesions.

K Boström; K E Watson; S Horn; C Wortham; I M Herman; L L Demer

doi:10.1172/JCI116391

Division of Cardiology, University of California, Los Angeles School of Medicine 90024-1679.

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Division of Cardiology, University of California, Los Angeles School of Medicine 90024-1679.

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Division of Cardiology, University of California, Los Angeles School of Medicine 90024-1679.

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Division of Cardiology, University of California, Los Angeles School of Medicine 90024-1679.

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Division of Cardiology, University of California, Los Angeles School of Medicine 90024-1679.

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Division of Cardiology, University of California, Los Angeles School of Medicine 90024-1679.

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Published in Volume 91, Issue 4 on April 1, 1993
J Clin Invest. 1993;91(4):1800–1809. https://doi.org/10.1172/JCI116391.
© 1993 The American Society for Clinical Investigation

Published April 1, 1993 - Version history

Artery wall calcification associated with atherosclerosis frequently contains fully formed bone tissue including marrow. The cellular origin is not known. In this study, bone morphogenetic protein-2a, a potent factor for osteoblastic differentiation, was found to be expressed in calcified human atherosclerotic plaque. In addition, cells cultured from the aortic wall formed calcified nodules similar to those found in bone cell cultures and expressed bone morphogenetic protein-2a with prolonged culture. The predominant cells in these nodules had immunocytochemical features characteristic of microvascular pericytes that are capable of osteoblastic differentiation. Pericyte-like cells were also found by immunohistochemistry in the intima of bovine and human aorta. These findings suggest that arterial calcification is a regulated process similar to bone formation, possibly mediated by pericyte-like cells.

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