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Submitted on May 15, 2003
Accepted on September 4, 2003
1 Institute of Animal Science Mariensee, (FAL), D-31535, Neustadt, Germany; Laboratory of Immunology, Gerontology Research Center, National Institute on Aging, NIH, 5600 Nathan Shock Drive, Baltimore, MD 21224
* To whom correspondence should be addressed. E-mail: Parvizi{at}tzv.fal.de.
Leptin is a key mediator of signals regulating food intake and energy expenditure and exerts potent immunomodulatory effects. We investigated the mechanisms mediating the action of leptin on GH secretion from peripheral blood mononuclear cells (PBMC). Using immunofluoresence microscopy we demonstrated a polarized expression pattern of leptin receptor protein on the surface of mononuclear cells, and constitutive expression of GH in PBMCs. Leptin exhibited a dose-dependent stimulatory effect on GH secretion by PBMC and also up-regulated the GH receptor gene expression. We did not observe any additive effects of leptin on GH secretion upon activation of cells with the plant mitogen PHA-M, unlike leptin, PHA-M exerted no effect on GH-R mRNA expression. Leptin lead to a nitric oxide synthase (NOS)-specific, dose-dependent increase in nitric oxide (NO) production from PBMCs, as leptin-induced NO release was blocked by the addition of the NOS inhibitor L-NAME and PKC inhibitor Calphostin-C. This leptin-induced GH secretion was dependent on both PKC and NO activation, as the addition of PKC and NOS inhibitors inhibited leptin-induced GH production. While the addition of sodium nitroprusside (SNP) a spontaneous liberator of NO, stimulated GH release from PBMCs, leptin had no additive or synergistic effect on SNP- induced GH production. Together, these findings demonstrate a unique action of leptin on immune cells via its ability to stimulate the GH production by blood mononuclear cells via PKC and NO-dependent pathways. These data also support a probable role for local immune-derived GH in mediating some of pleiotropic actions of leptin.
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