α-Melanocyte-stimulating hormone peptides inhibit HIV-1 expression in chronically infected promonocytic U1 cells and in acutely infected monocytes

Author:

Barcellini Wilma1,Colombo Gualtiero2,La Maestra Letteria1,Clerici Giuliana1,Garofalo Letizia2,Brini Anna T3,Lipton James M4,Catania Anna2

Affiliation:

1. Divisions of Hematology , Italy

2. Internal Medicine, Ospedale Maggiore di Milano IRCCS , 20122 Milano, Italy

3. Department of Pharmacology, Chemotherapy, and Toxicology, University of Milan , 20133 Milano, Italy

4. Zengen, Inc. , Woodland Hills, California

Abstract

Abstract The purpose of the present research was to determine if α-melanocyte-stimulating hormone (α-MSH) and its C-terminal tripeptide [α-MSH (11–13), KPV] alter HIV expression in infected cells. The results indicate that chronically HIV-1-infected promonocytic U1 cells produce α-MSH and that immunoneutralization of the endogenous peptide enhances HIV expression. Because U1 cells express the α-MSH receptor 1 (MC1R), an autocrine-inhibitory circuit based on the peptide and its receptor likely occurs in these cells. To determine effects of pharmacological concentrations of α-MSH peptides on HIV expression, we measured p24 antigen release by TNF-α-stimulated U1 cells exposed to a wide range of concentrations of synthetic α-MSH and KPV. Viral expression was reduced by both peptides. KPV also effectively reduced HIV replication in acutely infected monocyte-derived macrophages (MDM). The basis of the peptide influence on viral replication is at the transcriptional level; KPV inhibited activation of NF-κB that is known to enhance viral expression. Endogenous α-MSH likely contributes to natural defense against HIV. However, greater concentrations of synthetic peptide are much more effective in reducing HIV expression in infected cells.

Publisher

Oxford University Press (OUP)

Subject

Cell Biology,Immunology,Immunology and Allergy

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