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Related Experiment Videos

Fenofibrate activates AMPK and increases eNOS phosphorylation in HUVEC.

Hisashi Murakami1, Ryuichiro Murakami, Fukushi Kambe

  • 1Department of Cardiology, Nagoya University Graduate School of Medicine, 65 Tsurumai, Showa-ku, Nagoya 466-8550, Japan.

Biochemical and Biophysical Research Communications
|January 31, 2006
PubMed
Summary

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Fenofibrate enhances endothelial function by activating AMP-activated protein kinase (AMPK), leading to increased eNOS phosphorylation and nitric oxide (NO) production in human umbilical vein endothelial cells.

Area of Science:

  • Biochemistry
  • Molecular Biology
  • Cardiovascular Research

Background:

  • Fenofibrate is known to improve endothelial function via lipid-lowering and anti-inflammatory mechanisms.
  • Fenofibrate has been shown to upregulate endothelial nitric oxide synthase (eNOS).
  • AMP-activated protein kinase (AMPK) phosphorylates eNOS at Ser-1177, stimulating nitric oxide (NO) production.

Purpose of the Study:

  • To investigate whether fenofibrate activates AMPK and increases eNOS phosphorylation and NO production in human umbilical vein endothelial cells (HUVEC).

Main Methods:

  • Incubation of HUVEC with fenofibrate.
  • Assessing phosphorylation of AMPK and acetyl-CoA carboxylase.
  • Measuring eNOS phosphorylation and NO production.
  • Utilizing inhibitors of protein kinase A and phosphatidylinositol 3-kinase.

Related Experiment Videos

  • Testing other fibrates like bezafibrate and WY-14643.
  • Evaluating the requirement of transcriptional activities for AMPK activation.

    • Main Results:

    • Fenofibrate treatment increased the phosphorylation of AMPK and acetyl-CoA carboxylase in HUVEC.
    • Fenofibrate simultaneously enhanced eNOS phosphorylation and NO production.
    • Inhibitors of protein kinase A and phosphatidylinositol 3-kinase did not block fenofibrate-induced eNOS phosphorylation.
    • Bezafibrate and WY-14643 did not activate AMPK in HUVEC.
    • Fenofibrate activated AMPK independently of transcriptional activities.

    Conclusions:

    • Fenofibrate stimulates eNOS phosphorylation and NO production through the activation of AMPK.
    • This AMPK activation by fenofibrate is a novel characteristic of the agonist.
    • The mechanism is distinct from fenofibrate's effects on peroxisome proliferator-activated receptor alpha.