Modulation by leptin of proliferation and apoptosis in vascular endothelial cells

AIM: Plasma leptin concentrations not only correlate with body fat mass, but also with the degree of hypertensive retinopathy. The present study was designed to further examine, whether leptin's proliferative, proanglogenic activity relates to a yet uncovered anti-apoptotic effect. RESULTS: Leptin (10-50 nmol/l) concentration-dependently reduced apoptosis in HUVECs (human umbilical vein endothelial cells), HAVECs (human adult vein endothelial cells) and HMECs (human microvascular endothelial cells) by 20% (P less than or equal to 0.05). These findings were supported by increased expression of the apoptosis inhibitor bcl-2 (+55%, P<0.05) as well as by differential modulation of the respective cell cycle checkpoint genes/proteins p53 (-20%, P less than or equal to 0.01), p21(WAF-1/Cip1) (-23%, P less than or equal to 0.05) and the Retinoblastoma protein (+ 123%, P less than or equal to 0.01). CONCLUSION: bcl-2 dependent anti-apoptotic action might contribute to leptin's proanglogenic activity and thereby promote the development of vascular proliferative disease in obesity.