Research

Tissue Repair and Regeneration

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david.becker@ntu.edu.sg

David Becker

Prof 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 all 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 dozen patents and over 100 papers and book chapters. His professional experience includes evaluating research grants and fellowships for 19 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 $60M to commercialise the wound healing technology.  Currently Phase 2a clincal trials are underway on diabetic foot ulcers and Phase 2B trials have proven to be effective on venous leg ulcers.

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. Our 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. We 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. Our 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. We 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. We 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. We wish to understand the role of connexins in the formation and progression of these ulcers so that we can target them therapeutically.

 

Group Members

Dr Allyson Soon
Dr Shyan Low
Bhaarathy Velmurugan
Chua Jia Wang
Erica Teo Mei Ling
Liu Rubing
Milton Kwek
Leigh Edward Madden

Sutcliffe JE, Chin KY, Thrasivoulou C, Serena TE, O'Neil S, Hu R, White AM, Madden L, Richards T, Phillips AR, Becker DL. Abnormal connexin expression in human chronic wounds. Br J Dermatol. 2015 Aug 12. doi: 10.1111/bjd.14064 Link
Chowdhury B, David AL, Thrasivoulou C, Becker DL, Bader DL, Chowdhury TT. Tensile strain increased COX-2 expression and PGE2 release leading to weakening of the human amniotic membrane. Placenta. 2014 Dec;35(12):1057-64. doi:10.1016/j.placenta.2014.09.006. Link
O'Carroll SJ, Becker DL, Davidson JO, Gunn AJ, Nicholson LF, Green CR. The use of connexin-based therapeutic approaches to target inflammatory diseases. Methods Mol Biol. 2013;1037:519-46. doi: 10.1007/978-1-62703-505-7_31. Link
Rich T, Henderson LB, Becker DL, Cornell H, Patterson-Kane JC. Indicators of replicative damage in equine tendon fibroblast monolayers. BMC Vet Res. 2013 Sep 11;9:180. doi: 10.1186/1746-6148-9-180. Link
Balasubramaniyan V, Dhar DK, Warner AE, Vivien Li WY, Amiri AF, Bright B, Mookerjee RP, Davies NA, Becker DL, Jalan R. Importance of Connexin-43 based gap junction in cirrhosis and acute-on-chronic liver failure. J Hepatol. 2013 Jun;58(6):1194-200. doi: 10.1016/j.jhep.2013.01.023. Link
Davis NG, Phillips A, Becker DL. Connexin dynamics in the privileged wound healing of the buccal mucosa. Wound Repair Regen. 2013 Jul-Aug;21(4):571-8. doi: 10.1111/wrr.12054. Link
Gilmartin DJ, Alexaline MM, Thrasivoulou C, Phillips AR, Jayasinghe SN, Becker DL. Integration of scaffolds into full-thickness skin wounds: the connexin response. Adv Healthc Mater. 2013 Aug;2(8):1151-60. doi: 10.1002/adhm.201200357. Link
Mendoza-Naranjo A, Cormie P, Serrano AE, Hu R, O'Neill S, Wang CM, Thrasivoulou C, Power KT, White A, Serena T, Phillips AR, Becker DL. Targeting Cx43 and N-cadherin, which are abnormally upregulated in venous leg ulcers, influences migration, adhesion and activation of Rho GTPases. PLoS One. 2012;7(5):e37374. doi: 10.1371/journal.pone.0037374. Link
Mendoza-Naranjo A, Cormie P, Serrano AE, Wang CM, Thrasivoulou C, Sutcliffe JE, Gilmartin DJ, Tsui J, Serena TE, Phillips AR, Becker DL. Overexpression of the gap junction protein Cx43 as found in diabetic foot ulcers can retard fibroblast migration. Cell Biol Int. 2012 Jul;36(7):661-7. doi: 10.1042/CBI20110628. Link
Mendoza-Naranjo A, Bouma G, Pereda C, Ramírez M, Webb KF, Tittarelli A, López MN, Kalergis AM, Thrasher AJ, Becker DL, Salazar-Onfray F. Functional gap junctions accumulate at the immunological synapse and contribute to T cell activation. J Immunol. 2011 Sep 15;187(6):3121-32. doi: 10.4049/jimmunol.1100378. Link
Kaatz M, König K. [Multiphoton microscopy and in vivo tomography in dermatologic imaging]. Hautarzt. 2010 May;61(5):397-409. doi: 10.1007/s00105-009-1880-4. Link