The Effects of Adiponectin and Leptin on Human Endothelial Cell Proliferation: A Live-Cell Study

Abstract

The effect of adiponectin and leptin on the proliferation of the human microvascular endothelial cell line (HMEC-1) was studied in the absence or presence of fetal bovine serum (FBS). The participation of extracellular signal-regulated kinase (ERK) and phosphatidylinositol 3-kinase/Akt (PI-3K/Akt) pathways in this effect were evaluated. We studied the effect of both adipokines on the motility, mitosis, proliferation and cell death processes of HMEC-1 cells using live-cell imaging techniques. Adiponectin but not leptin further increased the proliferative effect induced by FBS on HMEC-1. This effect seems to be the consequence of an increase in the mitotic index in adiponectin-treated cells when compared to untreated ones. The presence of either the mitogen-activated protein kinase (MAPK) inhibitor (PD98059), or PI-3K inhibitor (LY294002), reduced the effect of adiponectin in a dose-dependent manner. Neither adipokine was able to affect HMEC-1 proliferation in FBS-free conditions. Duration of mitosis, cell motility and the cell death process were similar in all conditions. These data suggest that adiponectin and leptin exert different effects on endothelial cell function. Adiponectin was able to potentiate proliferation of HMEC-1. This effect involves the activation of both PI3-K/Akt and ERK/MAPK pathways. However, it seems to exert minimal effects on HMEC-1 function in the case of leptin.

Dihydroartemisinin inhibits endothelial cell proliferation through the suppression of the ERK signaling pathway

“…Activation of the ERK signaling pathway increases cell growth, and numerous extracellular stimuli regulates endothelial cell proliferation through manipulation of this pathway (9). Pre-treatment with PD98059 reduces endothelial cell proliferation induced by adiponectin, ghrelin and adropin (37)(38)(39). The present results confirmed the role of ERK signaling in mediating DHA-induced inhibition of endothelial cell proliferation.…”

T-cadherin Is Essential for Adiponectin-mediated Revascularization*

“…Thus, cell culture experiments were initiated to further delineate the functional relationship between T-cadherin and adiponectin. It has been reported previously that adiponectin promotes endothelial cell migration and proliferation in vitro (9,50,51). The dependence of in vitro angiogenic activities of adiponectin on T-cadherin expression in endothelial cells was evaluated.…”

Adiponectin improves coronary no-reflow injury by protecting the endothelium in rats with type 2 diabetes mellitus

“…Zhao et al [28] demonstrated that APN improved skeletal muscle microcirculation. Alvarez et al [29] found that APN promoted the proliferation of human endothelial cells. APN also inhibited the output of inflammatory cytokines and adhesion molecules, including intercellular adhesion molecule, vascular cell adhesion molecules, E-selectin on endothelial cells [30].…”