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Originally published In Press as doi:10.1074/jbc.C000629200 on October 3, 2000

J. Biol. Chem., Vol. 275, Issue 47, 36847-36851, November 24, 2000
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CLIF, a Novel Cycle-like Factor, Regulates the Circadian Oscillation of Plasminogen Activator Inhibitor-1 Gene Expression*

Koji MaemuraDagger §, Suzanne M. de la Monte, Michael T. ChinDagger , Matthew D. LayneDagger , Chung-Ming HsiehDagger , Shaw-Fang YetDagger , Mark A. PerrellaDagger ||, and Mu-En Leedagger Dagger

From the Dagger  Cardiovascular and the || Pulmonary and Critical Care Division, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115 and the  Department of Medicine and Pathology, Rhode Island Hospital, Brown University School of Medicine, Providence, Rhode Island 02903

The onset of myocardial infarction occurs frequently in the early morning, and it may partly result from circadian variation of fibrinolytic activity. Plasminogen activator inhibitor-1 activity shows a circadian oscillation and may account for the morning onset of myocardial infarction. However, the molecular mechanisms regulating this circadian oscillation remain unknown. Recent evidence indicates that basic helix-loop-helix (bHLH)/PAS domain transcription factors play a crucial role in controlling the biological clock that controls circadian rhythm. We isolated a novel bHLH/PAS protein, cycle-like factor (CLIF) from human umbilical vein endothelial cells. CLIF shares high homology with Drosophila CYCLE, one of the essential transcriptional regulators of circadian rhythm. CLIF is expressed in endothelial cells and neurons in the brain, including the suprachiasmatic nucleus, the center of the circadian clock. In endothelial cells, CLIF forms a heterodimer with CLOCK and up-regulates the PAI-1 gene through E-box sites. Furthermore, Period2 and Cryptochrome1, whose expression show a circadian oscillation in peripheral tissues, inhibit the PAI-1 promoter activation by the CLOCK:CLIF heterodimer. These results suggest that CLIF regulates the circadian oscillation of PAI-1 gene expression in endothelial cells. In addition, the results potentially provide a molecular basis for the morning onset of myocardial infarction.

* This work was supported by National Institutes of Health Grants HL 03745 (to M. T. C.), HL 10113 (to M. D. L.), HL 60788 (to M. A. P.), and HL 57664 (to M.-E. L.).The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.

The nucleotide sequence(s) reported in this paper has been submitted to the GenBankTM/EMBL Data Bank with accession number(s) AF256215.

dagger Deceased on April 10, 2000.

§ To whom correspondence should be addressed: Dept. of Cardiovascular Medicine, Graduate School of Medicine, University of Tokyo, Tokyo 113-8655, Japan. Fax: 81-3-5800-8824; E-mail: kmae-tky@umin. ac.jp.

Copyright © 2000 by The American Society for Biochemistry and Molecular Biology, Inc.
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