Modulation by leptin of proliferation and apoptosis in vascular endothelial cells.

Abstract

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, proangiogenic 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 < or = 0.05). These findings were supported by increased expression of the apoptosis inhibitor bcl-2 (+55%, P < or = 0.05) as well as by differential modulation of the respective cell cycle checkpoint genes/proteins p53 (-20%, P < or = 0.01), p21(WAF-1/Cip1) (-23%, P < or = 0.05) and the Retinoblastoma protein (+123%, P < or = 0.01).

CONCLUSION:

bcl-2 dependent anti-apoptotic action might contribute to leptin's proangiogenic activity and thereby promote the development of vascular proliferative disease in obesity.

• Authors: M Artwohl, M Roden, T Hölzenbein, A Freudenthaler, W Waldhäusl, S M Baumgartner-Parzer
• Journal: International journal of obesity and related metabolic disorders : journal of the International Association for the Study of Obesity (Int J Obes Relat Metab Disord) Vol. 26 Issue 4 Pg. 577-80 (Apr 2002) England
• PMID: 12075587 (Publication Type: Journal Article)

Chemical References

• Leptin
• Proto-Oncogene Proteins c-bcl-2
• RNA, Messenger

Topics

• Apoptosis (drug effects)
• Cell Division (drug effects)
• Cells, Cultured
• Endothelium, Vascular (cytology, drug effects)
• Female
• Gene Expression (drug effects)
• Genes, p53
• Humans
• Leptin (pharmacology)
• Microcirculation
• Proto-Oncogene Proteins c-bcl-2 (genetics)
• RNA, Messenger (analysis)
• Skin (blood supply)
• Umbilical Veins
• Uterus (blood supply)
• Veins