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Research Article Free access | 10.1172/JCI118543

H19, a marker of developmental transition, is reexpressed in human atherosclerotic plaques and is regulated by the insulin family of growth factors in cultured rabbit smooth muscle cells.

D K Han, Z Z Khaing, R A Pollock, C C Haudenschild, and G Liau

Department of Molecular Biology, Jerome H. Holland Laboratory, American Red Cross, Rockville, Maryland 20855, USA.

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Department of Molecular Biology, Jerome H. Holland Laboratory, American Red Cross, Rockville, Maryland 20855, USA.

Find articles by Khaing, Z. in: PubMed | Google Scholar

Department of Molecular Biology, Jerome H. Holland Laboratory, American Red Cross, Rockville, Maryland 20855, USA.

Find articles by Pollock, R. in: PubMed | Google Scholar

Department of Molecular Biology, Jerome H. Holland Laboratory, American Red Cross, Rockville, Maryland 20855, USA.

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Department of Molecular Biology, Jerome H. Holland Laboratory, American Red Cross, Rockville, Maryland 20855, USA.

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Published March 1, 1996 - More info

Published in Volume 97, Issue 5 on March 1, 1996
J Clin Invest. 1996;97(5):1276–1285. https://doi.org/10.1172/JCI118543.
© 1996 The American Society for Clinical Investigation
Published March 1, 1996 - Version history
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Abstract

H19 is a developmentally regulated gene with putative tumor suppressor activity, and loss of H19 expression may be involved in Wilms' tumorigenesis. In this report, we have performed in situ hybridization analysis of H19 expression during normal rabbit development and in human atherosclerotic plaques. We have also used cultured smooth muscle cells to identify H19 regulatory factors. Our data indicate that H19 expression in the developing skeletal and smooth muscles correlated with specific differentiation events in these tissues. Expression of H19 in the skeletal muscle correlated with nonproliferative, actin-positive muscle cells. In the prenatal blood vessel, H19 expression was both temporally and spatially regulated with initial loss of expression in the inner smooth muscle layers adjacent to the lumen. We also identified H19-positive cells within the adult atherosclerotic lesion and we suggest that these cells may recapitulate earlier developmental events. These results, along with the identification of the insulin family of growth factors as potent regulatory molecules for H19 expression, provide additional clues toward understanding the physiological regulation and function of H19.

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