Leptin requires canonical migratory signaling pathways for induction of monocyte and macrophage chemotaxis

• DOI: 10.1152/ajpcell.00062.2007
• Publication Date: 2007-08-30T01:00:48Z
• Authors: Marnie L. Gruen; Mingming Hao; David W. Piston; Alyssa H. Hasty
• Keywords: Leptin receptor

The growing worldwide obesity epidemic is frequently linked to an increased risk of developing diseases such as diabetes, cardiovascular disease, and cancer. These are associated with the infiltration macrophages in white adipose tissue (WAT), artery wall, tumors, respectively; these likely contribute disease progression pathogenesis. Abdominal WAT, surrounding heart well carcinoma cells, secrete many factors that could induce macrophage infiltration. Leptin adipocyte-secreted hormone, deficiency either leptin or its receptor has been shown cause morbid animals humans. However, what more commonly noted human presence central resistance leading hyperleptinemia. As receptors present on macrophages, we hypothesized act a monocyte/macrophage chemoattractant. Our current study demonstrates: 1) potent chemoattractant for monocytes inducing maximal chemotactic responses at 1 ng/ml; 2) leptin-mediated chemotaxis requires full-length migrating cells; 3) causes influx intracellular calcium macrophages; 4) activation janus kinase/signal transducers activators transduction (JAK/STAT), mitogen-activated protein kinase (MAPK), phosphatidylinositol 3-kinase (PI3K) pathways all necessary leptin-induced migration. Taken together, data demonstrate vitro canonical cell motility machinery activated upon exposure leptin. have implications impact hyperleptinemia obesity-related pathophysiological conditions