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Blood, 15 March 2006, Vol. 107, No. 6, pp. 2252-2261.
Prepublished online as a Blood First Edition Paper on November 29, 2005; DOI 10.1182/blood-2005-05-2011.
 Previous Article | Next Article 
Submitted May 19, 2005
Accepted November 7, 2005
Migration inhibitory factor upregulates vascular cell adhesion molecule-1 and intercellular adhesion molecule-1 via Src, PI3 kinase, and NF B
M A Amin, Christian S Haas, Kui Zhu, Pamela J Mansfield, Michael J Kim, Nicholas P Lackowski, and Alisa E Koch*
Department of Medicine, University of Michigan Medical School, Ann Arbor, Michigan, USA
Department of Medicine, Northwestern University Medical School, Chicago, Illinois, USA
Department of Medicine, University of Michigan Medical School, Ann Arbor, Michigan, USA; Veteran's Administration Chicago HealthCare Medical Center and Veteran's Administration, Ann Arbor, Michigan, USA
* Corresponding author; email: aekoch{at}umich.edu.
Cell adhesion molecules are critical in monocyte (MN) recruitment in immune-mediated and hematological diseases. We investigated the novel role of recombinant human migration inhibitory factor (rhMIF) in upregulating vascular cell adhesion molecule-1 (VCAM-1) and intercellular adhesion molecule-1 (ICAM-1) and their signaling pathways in human MNs. rhMIF-induced expression of VCAM-1 and ICAM-1 was significantly higher compared to nonstimulated MNs. rhMIF induced MN VCAM-1 and ICAM-1 expression in a concentration-dependent manner (p< 0.05). Antisense ODNs and inhibitors of Src, PI3K, p38, and NF B significantly reduced rhMIF-induced MN VCAM-1 and ICAM-1 expression (p< 0.05). However, Erk1/2 and Jak2 were not involved. Silencing RNA directed against MIF, and inhibitors of Src, PI3K, NFB, anti-VCAM-1 and anti-ICAM-1 significantly inhibited rhMIF-induced adhesion of HL-60 cells to human dermal microvascular endothelial cells (HMVECs) or an endothelial cell line, HMEC-1 in cell adhesion assays, suggesting the functional significance of MIF-induced adhesion molecules (p< 0.05). rhMIF also activated MN phospho-Src, -Akt, and -NFB in a time-dependent manner. rhMIF induced VCAM-1 and ICAM-1 upregulation in 12 hours via Src, PI3K, and NFB as shown by Western blotting and immunofluoresecence. MIF and MIF-dependent signaling pathways may be a potential target for treating diseases characterized by upregulation of cell adhesion molecules.
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