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Moderate dose insulin promotes function of endothelial progenitor cells
Author(s) -
Zhao Li,
Cao Feng,
Yin Tao,
Sun Dongdong,
Cheng Kang,
Zhang Jun,
Wang Haichang
Publication year - 2011
Publication title -
cell biology international
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.932
H-Index - 77
eISSN - 1095-8355
pISSN - 1065-6995
DOI - 10.1042/cbi20100205
Subject(s) - insulin , enos , medicine , endocrinology , progenitor cell , protein kinase b , bone marrow , endothelial progenitor cell , nitric oxide , endothelium , insulin receptor , downregulation and upregulation , nitric oxide synthase , biology , phosphorylation , stem cell , insulin resistance , microbiology and biotechnology , biochemistry , gene
EPCs (endothelial progenitor cells) regenerate the vascular endothelial cells and keep the integrity of the vascular endothelium and thus may retard the onset of atherosclerosis. Steady state levels of EPCs in the circulation were found to be correlated with cardiovascular event risks. Given the close relationship between insulin and the cardiovascular system, we tested the long‐term effects of moderate‐dose insulin treatment on bone marrow‐derived EPCs. Rat bone marrow EPCs were exposed to various levels of insulin under normal (5 mmol/l) or high (40 mmol/l) glucose conditions for 7 days. Insulin at levels near the physiological range (0.1, 1 nmol/l) up‐regulated EPCs proliferation, stimulated NO (nitric oxide) production and reduced EPC senescence and ROS (reactive oxygen species) generation under both normal‐ and high‐glucose conditions. Glucose exerted deleterious effects on EPCs contrary to insulin. Western blot analysis suggested concomitant decrease of Akt phosphorylation and eNOS (endothelial nitric oxide synthase) expression by high‐glucose treatment and increase with insulin administration. Thus, insulin promoted several activities of EPCs, which suggested a potential endothelial protective role of insulin. Akt/eNOS pathway may be involved in the modulation of EPCs function by glucose and insulin.