||Professor David Becker|
Professor of Tissue Repair and Regeneration
Principal Investigator, Tissue Repair and Regeneration Laboratory
- Leigh Madden, Research Associate
- Chua Jia Wang, PhD Student
- Kwek Sheng Yi Milton, PhD Student
- Erica Teo Mei Ling, PhD Student
- Zi Xin Ong, PhD Student
Professor David Becker is Professor in Tissue Repair and Regeneration at Lee Kong Chian School of Medicine, Nanyang Technological University. Prior to this appointment, Prof Becker spent most of his scientific career at the world-renowned University College London (UCL), UK. After obtaining his PhD at UCL in 1988, he worked as a Research Fellow there until he was awarded a prestigious 10 year Royal Society University Research Fellowship in 1994. He was made a Lecturer at UCL in 1999, Reader in 2005 and Full Professor in 2008.
Prof Becker is internationally recognised for his contributions to the biology of gap junctional communication in development and disease. He has provided fundamental insights into the regulation of connexins in wounded skin and contributed to the discovery of ways to speed up acute wound healing whilst reducing inflammation and scar formation; and more importantly kicking start healing when it has stalled as in the case of chronic ulcers. This work has resulted in a thirty patents and over 100 papers and book chapters.
His professional experience includes evaluating research grants and fellowships for over twenty international funding bodies including the Wellcome Trust, MRC, BBSRC, NSF and NHS. His work is highly relevant as it is translational in the field of chronic wounds where there is a large unmet medical need. He has won several awards for his business plans and these, along with the science, supported the formation of a biotech company, CoDaTherapeutics, which has raised over $70M to commercialise the wound healing technology. Phase 2a clincal trials on diabetic foot ulcers and Phase 2B trials on venous leg ulcers have proven to be effective.
Connexins" The general interest of the lab relate to the biology of gap junctions and the contribution of different connexins to the pathology of wound healing in acute and chronic conditions. Prof Becker’s lab aim is to understand the roles of different connexins in the healing process and to determine the expression levels that allow optimal healing to take place.
Biofilms: Many chronic wounds are infected with bacteria and often have substantial build up of biofilms. Prof Becker and his team are attempting to dissect out the effects of different biofilm components on connexin expression and wound healing in a variety of in vitro and in vivo models.
Scaffolds: Engineered scaffolds are used to replace missing tissues in ulcers and burns with the intention to encourage cells to invade the scaffold and reform new tissue. Their studies have shown that cells at the wound edge in contact with the scaffolds undergo a foreign body reaction and fail to migrate and integrate with the scaffold. They are now investigating ways of bioactivating scaffolds in order to make them more compatible with surrounding tissues in order to promote integration and wound healing.
Chronic wounds: Protein expression patterns in chronic wounds are often at levels many fold greater than in normal tissues or wounds. They wish to identify the misexpressed proteins that have a negative effect on the healing process and to target them for therapeutic benefit.
Pressure Ulcers: These is a significant problem for the growing elderly population and is found in between 12-25% of the elderly in care homes or geriatric wards. They wish to understand the role of connexins in the formation and progression of these ulcers so that we can target them therapeutically.
Qiu, C., Coutinho, P., Frank, S., Franke, S., L-Y. Law, Martin, P., Green, C.R. and Becker D.L. (2003) Accelerated rate of wound repair by targeting connexin 43 expression. Current Biology 13, 1697-1703
Coutinho, P., Qiu, C., Frank, S., Tamber, K. and Becker D.L (2003) Key events in the wound healing process correlate with changes in connexin expression. Cell Biol. Int. 27, 525-541.
Marziano, N., Casalotti, S.O, Portelli A.E., Becker, D.L. and Forge, A. (2003) Deafness-related mutations in gap junction protein connexin 26 have a dominant negative effect on connexin 30. Human Molecular Genetics 203, 805-812.
Coutinho, P., Frank, S., Qiu, C., CM., Wang, Brown, T., Green, C.R. and Becker D.L. (2005) Limiting burn extension by transient inhibition of Connexin43 expression at the site of injury Brit. J. Plast. Surg. 58, 658-667.
Theodossiou, TA., Thrasivoulou, C., Ekwobi, C and Becker D.L. (2006) Second harmonic generation confocal microscopy of collagen type I from rat tendon cryosections. Biophysics Journal 91, 4665-4677.
Mori, R., Power, K., Wang, CM., Martin P. and Becker, D.L. (2006) Acute downregulation of connexin43 at wound sites leads to a reduced inflammatory response along with enhanced keratinocytes proliferation and fibroblast migration. J. Cell Sci. 119, 5193-5203.
Wang, CM., Lincoln, J., Cook, J.E. and Becker, DL. (2007) Abnormal connexin expression underlies delayed wound healing in diabetic rat skin. Diabetes 56, 2809-2817.
Cronin, M., Anderson, P., Cook, J.E., Green, CR. and Becker, D.L. (2008) Targeting connexin 43 following rat spinal cord injury reduces inflammation and improves functional recovery. Molecular Cellular Neurosci. 39, 152-60.
Sutcliffe, JES, Chin, KY, Thrasivoulou, C., Serena, TE, O’Neil, S, Hu, R, Wright JA., Richards, T., Phillips, ARJ. and Becker, DL. (2015) Abnormal Connexin expression in chronic wounds may impair healing. British Journal of Dermatology 173, 1205-1215.
Gilmartin, DJ, Soon, A, Thrasivoulou, C, Phillips, ARJ, Jayasinghe, SN and Becker, DL. (2016) Sustained Release of Cx43 Antisense Oligodeoxynucleotides from Coated Collagen Scaffolds Promotes Wound Healing. Advanced Healthcare Materials 5, 1786-99.