Key result
MIF antagonist ISO-1 reduces endometriotic implant size and vascularity in mice.
Why the study?
The functional role of macrophage migration inhibitory factor (MIF) in the pathogenesis of endometriosis is uncertain.
Does the MIF antagonist ISO-1 reduce endometriotic implant size in mice with experimentally induced endometriosis?
Does the MIF antagonist ISO-1 reduce endometriotic implant size in mice with experimentally induced endometriosis?
Inhibition of MIF activity with ISO-1 significantly reduces endometriotic implant size and vascularity in a mouse model, suggesting MIF as a potential therapeutic target for endometriosis.
ISO-1 reduces lesions in a murine model; hypothesis-generating for MIF inhibition in human endometriosis.
Aim Macrophage migration inhibitory factor (MIF) is a cytokine whose expression is elevated in endometriotic tissue from women with the disease but the functional role of this factor in the pathogenesis of the disease is uncertain. The objective of the current study was to examine the role of MIF in the pathogenesis of endometriosis. Method Experimental endometriosis was induced in mice and the ability of the MIF antagonist, ISO-1, to reduce endometriotic implant size was assessed. Results Administration of ISO-1 resulted in a significant reduction in implant size and vascularity (as assessed by Flk1 mRNA expression) which was not associated with an alteration in the reproductive cycle. Conclusion These data suggest that inhibition of MIF activity is associated with a significant reduction in endometriotic implant size and leads us to speculate that a similar approach of targeting MIF may prove useful in treating endometriosis in humans.
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Nothnick et al. (2011) studied Endometriosis. MIF antagonist, ISO-1 was evaluated on Endometriotic implant size and vascularity. Administration of the MIF antagonist ISO-1 significantly reduced endometriotic implant size and vascularity in mice with experimentally induced endometriosis.
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