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BioMed Research International
Volume 2013 (2013), Article ID 941764, 13 pages
http://dx.doi.org/10.1155/2013/941764
Research Article

Neurotensin Modulates the Migratory and Inflammatory Response of Macrophages under Hyperglycemic Conditions

1Center for Neuroscience and Cell Biology, University of Coimbra, 3004-517 Coimbra, Portugal
2CIEPQPF, Chemical Engineering Department, FCTUC, University of Coimbra, 3030-790 Coimbra, Portugal
3Faculty of Pharmacy, University of Coimbra, 3000-548 Coimbra, Portugal
4The Portuguese Diabetes Association (APDP), Rua Do Salitre, No. 118-120, 1250-203 Lisboa, Portugal

Received 8 April 2013; Revised 24 June 2013; Accepted 28 June 2013

Academic Editor: Senthil K. Venugopal

Copyright © 2013 Liane I. F. Moura et al. This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

Abstract

Diabetic foot ulcers (DFUs) are characterized by an unsatisfactory inflammatory and migratory response. Skin inflammation involves the participation of many cells and particularly macrophages. Macrophage function can be modulated by neuropeptides; however, little is known regarding the role of neurotensin (NT) as a modulator of macrophages under inflammatory and hyperglycemic conditions. RAW 264.7 cells were maintained at 10/30 mM glucose, stimulated with/without LPS (1 μg/mL), and treated with/without NT(10 nM). The results show that NT did not affect macrophage viability. However, NT reverted the hyperglycemia-induced impair in the migration of macrophages. The expression of IL-6 and IL-1β was significantly increased under 10 mM glucose in the presence of NT, while IL-1β and IL-12 expression significantly decreased under inflammatory and hyperglycemic conditions. More importantly, high glucose modulates NT and NT receptor expression under normal and inflammatory conditions. These results highlight the effect of NT on cell migration, which is strongly impaired under hyperglycemic conditions, as well as its effect in decreasing the proinflammatory status of macrophages under hyperglycemic and inflammatory conditions. These findings provide new insights into the potential therapeutic role of NT in chronic wounds, such as in DFU, characterized by a deficit in the migratory properties of cells and a chronic proinflammatory status.