August 9, 2004FEBS LettersOpen Access

Thrombin and histamine stimulate endothelial nitric‐oxide synthase phosphorylation at Ser1177 via an AMPK mediated pathway independent of PI3K‐Akt

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Population

Human umbilical vein endothelial cells (HUVECs)

Comparison

Thrombin and histamine, along with various… vs Untreated or differently treated cells

Design

Preclinical

Authors

Discussion

Suggests AMPK as alternative eNOS regulator in endothelium; hypothesis-generating and should not yet influence clinical practice.

Population

Human umbilical vein endothelial cells (HUVECs)

Intervention

Thrombin and histamine, along with various kinase inhibitors (H89, Rp-cAMPS) and activators (AICAR, CCCP)

Comparator

Untreated or differently treated cells

Outcome

Phosphorylation and activation of endothelial NO-synthase (eNOS) on Ser1177surrogate

Thrombin and histamine stimulate eNOS phosphorylation via an AMPK-mediated pathway rather than the PI3K-Akt pathway in human endothelial cells.

Thors et al. (2004) studied this question.

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