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Transient High-Glucose Exposure and Erk Signaling.

Junichi Okada1, Tsugumichi Saito2, Eijiro Yamada2

  • 1Department of Medicine, Division of Endocrinology, Albert Einstein College of Medicine Bronx, NY USA.

Circulation Reports
|January 12, 2026
PubMed
Summary

Transient high glucose activates Erk2 in human coronary artery endothelial cells (HCAEC) via a specific signaling pathway. This finding offers potential therapeutic targets for atherosclerosis.

Keywords:
Coronary artery endothelial cellsGiα2Rap1RasmiR-138

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Area of Science:

  • Cardiovascular Biology
  • Molecular Cell Biology
  • Endothelial Cell Function

Background:

  • Transient high-glucose exposure is known to induce Erk2 phosphorylation and proliferation in human coronary artery endothelial cells (HCAEC).
  • The precise upstream molecular mechanisms driving this response in HCAEC remain largely unelucidated.

Purpose of the Study:

  • To investigate the signaling pathways mediating Erk2 activation in HCAEC following transient high-glucose exposure.
  • To identify key molecular players involved in the response of HCAEC to hyperglycemia.

Main Methods:

  • Human coronary artery endothelial cells (HCAEC) were subjected to transient exposure (1 hour) of high D-glucose (183 mg/dL) followed by a period in glucose-free medium.
  • Analysis included assessment of microRNA-138 (miR-138) levels, Giα2 protein expression, and the activity of Rap1 and Ras signaling proteins.

Main Results:

  • Transient high D-glucose significantly decreased miR-138 levels in HCAEC.
  • This was accompanied by an increase in Giα2 protein levels.
  • The signaling cascade involved inactivation of Rap1 and activation of Ras, ultimately leading to Erk2 activation.

Conclusions:

  • Transient high D-glucose activates Erk2 in HCAEC through a specific signaling axis involving miR-138, Giα2, Rap1, and Ras.
  • This miRNA-138/Giα2/Rap1/Ras pathway represents a potential therapeutic target for managing conditions like atherosclerosis.