Please use this identifier to cite or link to this item: http://hdl.handle.net/2440/78707
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Type: Journal article
Title: The influence of Flightless I on toll-like-receptor-mediated inflammation in a murine model of diabetic wound healing
Author: Ruzehaji, N.
Mills, S.
Melville, E.
Arkell, R.
Fitridge, R.
Cowin, A.
Citation: BioMed Research International, 2013; 2013:389792-1-389792-9
Publisher: Hindawi Publishing Corporation
Issue Date: 2013
ISSN: 2314-6133
2314-6141
Statement of
Responsibility: 
Nadira Ruzehaji, Stuart J. Mills, Elizabeth Melville, Ruth Arkell, Robert Fitridge and Allison J. Cowin
Abstract: Impaired wound healing and ulceration represent a serious complication of both type 1 and type 2 diabetes. Cytoskeletal protein Flightless I (Flii) is an important inhibitor of wound repair, and reduced Flii gene expression in fibroblasts increased migration, proliferation, and adhesion. As such it has the ability to influence all phases of wound healing including inflammation, remodelling and angiogenesis. Flii has the potential to modulate inflammation through its interaction with MyD88 which it an adaptor protein for TLR4. To assess the effect of Flii on the inflammatory response of diabetic wounds, we used a murine model of streptozocin-induced diabetes and Flii genetic mice. Increased levels of Flii were detected in Flii transgenic murine wounds resulting in impaired healing which was exacerbated when diabetes was induced. When Flii levels were reduced in diabetic wounds of Flii-deficient mice, healing was improved and decreased levels of TLR4 were observed. In contrast, increasing the level of Flii in diabetic mouse wounds led to increased TLR4 and NF-κB production. Treatment of murine diabetic wounds with neutralising antibodies to Flii led to an improvement in healing with decreased expression of TLR4. Decreasing the level of Flii in diabetic wounds may therefore reduce the inflammatory response and improve healing.
Keywords: Animals; Humans; Mice; Diabetes Mellitus, Experimental; Diabetes Mellitus, Type 1; Diabetes Mellitus, Type 2; Diabetes Complications; Wounds and Injuries; Disease Models, Animal; Inflammation; Carrier Proteins; Cytoskeletal Proteins; NF-kappa B; Wound Healing; Gene Expression Regulation; Toll-Like Receptor 4; Myeloid Differentiation Factor 88
Rights: Copyright © 2013 Nadira Ruzehaji 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.
RMID: 0020126521
DOI: 10.1155/2013/389792
Grant ID: http://purl.org/au-research/grants/nhmrc/1002009
Appears in Collections:Paediatrics publications

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