Effects of reduced β2 glycoprotein I on high glucose-induced cell death in HUVECs

Reduced beta 2 glycoprotein I (beta 2GPI) has been demonstrated to exhibit a beneficial effect in diabetic atherosclerosis and retinal neovascularization. However, the effect of reduced beta 2GPI on vascular disorders in diabetic mellitus (DM) remains to be elucidated. The present study established a high glucose-induced injury model using human umbilical cords veins (HUVECs) and evaluated the protective effects of reduced beta 2GPI against the injury. The data demonstrated that a low concentration of reduced beta 2GPI (0.5 mu M) mitigated high glucose-induced cell loss, decreased nitric oxide (NO) production and resulted in calcium overloading. Mechanically, reduced beta 2GPI additionally reversed high glucose-induced phosphatase and tensin homolog (PTEN) accumulation, decrease of protein kinase B phosphorylation and nitric oxide synthase activity, and increase of cyclooxygenase-2 activity. It was further confirmed that PTEN inhibitor-bpV (1 mu M) exhibited similar effects to those resulting from reduced beta 2GPI. Overall, the data revealed that reduced beta GPI exerts protective effects from glucose-induced injury in HUVECs, potentially via decreasing PTEN levels. The present study suggests reduced beta 2GPI may act as a novel therapeutic strategy for the treatment of vascular disorders in DM.