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-/- mice and restoration of function by exogenous MIP-1
1 Department of Physiology, University of Kentucky, Lexington, KY, USA
2 Department of Anatomy and Neurobiology, University of Kentucky, Lexington, KY, USA
3 Department of Statistics, University of Kentucky, Lexington, KY, USA
4 Sanders-Brown Center on Aging, University of Kentucky, Lexington, KY, USA
5 Department of Anatomy and Neurobiology, University of Kentucky, Lexington, KY, USA; Sanders-Brown Center on Aging, University of Kentucky, Lexington, KY, USA
6 Department of Physiology, University of Kentucky, Lexington, KY, USA; Sanders-Brown Center on Aging, University of Kentucky, Lexington, KY, USA
* To whom correspondence should be addressed. E-mail: tgetche{at}uky.edu.
The chemokine macrophage inflammatory protein (MIP)-1
recruits macrophages to sites of epithelial remodeling. We showed previously that mRNA and protein levels of MIP-1 in the olfactory epithelium (OE) increased significantly at 3 d after bilateral olfactory bulbectomy (OBX). The first aim of this study was to investigate the effect of the absence of MIP-1 on macrophage recruitment to the OE 3 d after OBX in Mip-1-/- mice compared to C57BL/6 mice and to test if chemokine function could be restored by MIP-1-protein injection into Mip-1-/- mice. OBX was performed on C57BL/6 and Mip-1-/- mice. The mice received 6 injections (s.c.) at 12-h intervals of either 10 µg/ml MIP-1 protein in carrier or carrier only. Macrophage recruitment was evaluated with antibodies to CD68 for all macrophages and F4/80 for activated macrophages. Compared to C57BL/6 mice, at 3 d post-OBX the numbers of CD68+ and F4/80+ macrophages were significantly lower in carrier-injected Mip-1-/- mice and were comparable in MIP-1 protein-injected Mip-1-/- mice. The second aim was to determine the identity of genes regulated at 3 d post-OBX in the OE of carrier-injected Mip-1-/- mice compared with carrier-injected C57BL/6 mice. Total RNA from the OE was hybridized to Affymetrix microarrays. A number of chemokine-, cytokine-, and growth factor-related genes were significantly regulated in the Mip-1-/- mice, and were restored in MIP-1 protein-injected Mip-1-/- mice. The results illustrated that MIP-1 played a key role in recruitment of macrophages to the OE and provided insight into the genomic regulation involved in OE remodeling.
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