Effect of thymosin beta 4 in the presence of up-regulation of the insulin-like growth factor-1 signaling pathway on high-glucose-exposed vascular endothelial cells.

Thymosin beta 4 (Tβ4), which regulates vascular cell growth, can ameliorate some of the problems associated with diabetes. However, the precise signaling mechanisms by which Tβ4 protects against hyperglycemia-induced damage to endothelial cells have not been investigated in detail. Thus, the aim of this study was to elucidate the role of Tβ4 in diabetes and the possible involvement of insulin-like growth factor-1 (IGF-1), which affects cellular survival, metabolism, and glucose homeostasis in high-glucose (HG)-injured human umbilical vein endothelial cells (HUVECs). Immunoblotting assays revealed that under HG blockade conditions, Tβ4 did not alter the insulin-signaling pathway, but induced overexpression of IGF-1 protein, leading to activation of factors in alternative signaling pathway. Small interfering RNA of Tβ4 and IGF-1 were studied to clarify relationship between Tβ4 and IGF-1. These findings suggest that IGF-1 induction by Tβ4 ameliorates the damage in HG-injured HUVECs which manifest as diabetic vascular disorder.