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Parallel Measurement of Circadian Clock Gene Expression and Hormone Secretion in Human Primary Cell Cultures
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Plasminogen activator inhibitor-1 and the circadian clock in metabolic disorders

Katsutaka Oishi1

  • 1Clock Cell Biology Research Group, Institute for Biological Resources and Functions, National Institute of Advanced Industrial Science and Technology, Central 6, 1-1-1 Higashi, Tsukuba, Ibaraki, Japan. k-ooishi@aist.go.jp

Clinical and Experimental Hypertension (New York, N.Y. : 1993)
|April 24, 2009
PubMed

Insights

Circadian clock proteins regulate plasminogen activator inhibitor-1 (PAI-1) gene expression, impacting morning hypofibrinolysis. This circadian rhythm is vital for metabolic health, particularly in obesity and diabetes.

Area of Science:

  • Chronobiology
  • Molecular Biology
  • Physiology

Background:

  • Plasma levels of plasminogen activator inhibitor-1 (PAI-1) exhibit significant circadian fluctuations, leading to hypofibrinolysis in the early morning.
  • The circadian expression of the PAI-1 gene is primarily controlled by core circadian clock proteins, including CLOCK and BMAL1/BMAL2.

Purpose of the Study:

  • To investigate the role of circadian clock proteins in regulating PAI-1 expression and its impact on fibrinolysis.
  • To explore the connection between circadian clock proteins, PAI-1, and metabolic disorders like obesity and diabetes.

Main Methods:

  • Analysis of plasma PAI-1 levels in diurnal and nocturnal species to establish circadian patterns.
  • Investigating the regulatory mechanisms of PAI-1 gene expression by circadian clock proteins.

Main Results:

  • Plasma PAI-1 levels show a consistent increase at the onset of the active phase in both humans and rodents.
  • Circadian clock proteins are crucial for the hypofibrinolytic state associated with metabolic disorders such as obesity and diabetes.

Conclusions:

  • Rhythmic PAI-1 expression, driven by circadian clock proteins, is essential for physiological processes across species.
  • Circadian clock proteins play a significant role in the hypofibrinolysis observed in metabolic diseases, highlighting potential therapeutic targets.

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