Moderate dose insulin promotes function of endothelial progenitor cells

Area of Science:

• Cardiovascular Biology
• Endothelial Cell Biology
• Metabolic Disease Research

Background:

• Endothelial progenitor cells (EPCs) are crucial for vascular repair and maintaining endothelial integrity, potentially delaying atherosclerosis.
• Circulating EPC levels are linked to cardiovascular event risks.
• Insulin has known cardiovascular effects, prompting investigation into its impact on EPCs.

Purpose of the Study:

• To investigate the long-term effects of moderate-dose insulin on bone marrow-derived EPCs.
• To determine if insulin influences EPC proliferation, senescence, nitric oxide production, and reactive oxygen species generation.
• To explore the role of the Akt/eNOS pathway in insulin's modulation of EPC function.

Main Methods:

• Rat bone marrow EPCs were cultured for 7 days.
• Cells were exposed to varying insulin concentrations under normal (5 mmol/l) and high (40 mmol/l) glucose conditions.
• EPC proliferation, senescence, nitric oxide (NO) production, reactive oxygen species (ROS) generation, Akt phosphorylation, and endothelial nitric oxide synthase (eNOS) expression were assessed.

Main Results:

• Physiological insulin levels (0.1, 1 nmol/l) increased EPC proliferation and NO production while decreasing senescence and ROS generation.
• These beneficial effects of insulin were observed under both normal and high glucose conditions.
• High glucose negatively impacted EPCs, whereas insulin counteracted these effects, increasing Akt phosphorylation and eNOS expression.

Conclusions:

• Insulin promotes EPC proliferation, NO production, and reduces senescence and ROS, indicating a potential endothelial protective role.
• The Akt/eNOS pathway is implicated in how glucose and insulin modulate EPC function.
• Insulin may offer cardiovascular protection by enhancing EPC activity.