Wounds, burns and scalds are frequent injuries which can lead to deformity, disfigurement and loss of movement. We have shown that the cytoskeletal protein, Flightless I (FliI), is an important regulator of wound repair. We plan to further investigate FliI in wound and burn injuries using new cell-specific transgenic animal models and to develop a new FliI-antibody based therapy to treat wound and burn injuries.
Development Of Flightless Antibody Therapy For Treating Wounds
Funder
National Health and Medical Research Council
Funding Amount
$194,071.00
Summary
Chronic wounds, diabetic ulcers, injuries in response to trauma, burns and scalds form a medical need which will only expand as the population ages and the diabetic epidemic grows. In our studies, we have shown that Flightless I (FliI), an actin-remodelling protein, is a negative regulator of incisional wound healing. We are now developing a new antibody therapy to reduce FliI levels in wounds thereby leading to improved wound repair outcomes.
Function Of Flightless I In The Skin Blistering Disorder Epidermolysis Bullosa
Funder
National Health and Medical Research Council
Funding Amount
$578,796.00
Summary
Skin blistering disorders are painful and debilitating. They can lead to permanent scarring and may be life threatening within two years of birth. No specific cure exists. Our previous studies have identified the important role of Flii in wound healing. We now aim to investigate the potential function of Flii in skin blistering disorders. We will also determine whether modulating Flii reduces blister formation. This research could lead to new therapies for treating people with fragile skin.
Mechanism Of Flightless I Function In Burn Injury And Scar Formation
Funder
National Health and Medical Research Council
Funding Amount
$545,216.00
Summary
Extensive scarring is a major clinical problem often resulting from burn injuries. We have previously shown that the cytoskeletal protein, Flightless I (FliI), is an important regulator of wound repair. We now plan to investigate whether FliI is also be the mechanistic link between cytoskeletal remodelling and induction of TGF-betas post-wounding leading to scar formation.