Schulich school of Medicine and Dentistry logo Department of Anatomy and Cell Biology Schulich School of Medicine & Dentistry

Dr. Dale W. Laird

laird

Professor and Canada Research Chair in Gap Junctions and Disease
(Cross Appointment with Physiology and Pharmacology)

Ph.D. University of British Columbia
M.Sc. University of British Columbia
B.Sc. University of Prince Edward Island

Office: 00077 Dental Sciences Building
Phone: 519-661-2111 Ext. 86827
Fax: 519-850-2562
Email: Dale.Laird@schulich.uwo.ca
Visit: Dr. Laird's Home Page

Research Interests:

Dr. Laird’s research program focuses on the role of gap junctions in human health and disease. Mutations in ten genes that encode members of the connexin family of gap junction proteins lead to a wide range of human diseases that include developmental disorders, hearing loss, skin defects and neuropathies. Moreover, the ability of connexins to control the growth of cancer cells led to connexins being defined as tumor suppressors. Dr. Laird’s research centers around three themes related to normal connexin assembly and turnover, defects in disease-causing connexin mutants and mechanisms of connexin down-regulation in human breast cancer. These studies have expanded in recent years to encompass a second class of channel forming proteins called pannexins. Experimental approaches in each of these focal areas rely on biochemical, molecular, histological and cell imaging technologies. In addition, Dr. Laird’s team actively uses several mutant mouse models of connexin-linked human diseases and has now developed novel human models of human disease where wet-bench research findings are correlated with the clinical setting. His research program is currently funded by grants from the Canadian Institutes of Health Research, the Canadian Breast Cancer Research Alliance, the Canada Research Chairs Program and the Canadian Foundation for Innovation.

Selected Publications:

  1. Q. Shao, K. Lindstrom, R. Shi, J. Kelly, A. Schroeder, J. Juusola, K. Levine, J.L. Esseltine, S. Penuela, M.F. Jackson and D.W. Laird (2016) "A germline variant in PANX1 is associated with intellectual disability and multisystem dysfunction" Journal of Biological Chemistry 291: 12432-12443. Featured as: “Paper of the Week”

  2. D. Caskenette, S. Penuela, V. Lee, K. Barr, F. Beier, D.W. Laird* and K.E. Willmore* (2016) “Global deletion of Panx3 produces multiple phenotypic effects in mouse humeri and femora” Journal of Anatomy 228: 746-756. *Co-corresponding authors.

  3. J.J. Kelly, J. Esseltine, Q. Shao, E.W. Jabs, J. Sampson, M. Auranen, D. Bai and D.W. Laird (2016) “Specific functional pathologies of Cx43 mutations associated with oculodentodigital dysplasia” Molecular Biology of the Cell 27: 2172-2185

  4. M. Siddiqui, S. Swarbreck, Q. Shao, D. Secor, T. Peng, D.W. Laird and K. Tyml (2016) “Critical role of Cx40 in reduced endothelial electrical coupling by lipopolysaccharide and hypoxia reoxygenation” Journal of Vascular Research 52: 396-403.

  5. M.K.G. Stewart, I. Plante, S. Penuela and D.W. Laird (2016) “Loss of Panx1 impairs mammary gland development at lactation: implications for breast tumorigenesis” PLoS One 11(4):e0154162. doi: 10.1371

  6. J.L. Esseltine, Q. Shao, T. Huang, J.J. Kelly, J. Sampson and D.W. Laird (2015) “Manipulating Cx43 expression triggers gene reprogramming events in dermal fibroblasts from oculodentodigital dysplasia patients” Biochemical Journal 472: 55-69.

  7. M.K.G. Stewart, J. Simek and D.W. Laird (2015) “Insights into the role of connexins in mammary gland morphogenesis and function” Reproduction 149:R279-R290.

  8. J.J. Kelly, J. Simek and D.W. Laird (2015) “Mechanisms linking connexin mutations to human diseases” Cell and Tissue Research 360: 701-721.

  9. J.J. Kelly, Q. Shao, D.J. Jagger and D.W. Laird (2015) “Cx30 exhibits unique characteristics including a long half-life when assembled into gap junctions” Journal of Cell Science 128: 3947-3960. Highlighted “In this Issue”

  10. M.K.G. Stewart, J.F. Bechberger, I. Welch, C.C. Naus and D. W. Laird (2015) “Cx26 knockdown predisposes the mammary gland to primary mammary tumors in a DMBA-induced mouse model of breast cancer” Oncotarget 6: 37185-37199.

  11. R. Nahta, F. Al-Mulla, R. Al-Temaimi, A. Amedie, R. Andrade-Vieira, S. Bay, D. Brown, G. Calaf, R.C. Castellino, K.A. Chone-Solal, N. Cruickshanks, P. Dent, R. Di Fiore, St. Forte, G.S. Goldberg, R. A. Hamid, H. Krishnan, D.W. Laird, A. Lasfar, P. Marignani, L. Memeo, C. Mondello, C.C. Naus, R. Ponce-Cusi, J. Raju, D. Roy, R. Roy, E. Ryan, H.K. Salem, I. Scovassi, N. Singh, M. Vaccari, R. Vento, J. Vondracek, M. Wade, J. Woodrick and W. H. Bisson (2015) “Mechanisms by which cancer cells evade growth suppression and the potential molecular effects of selected environmental chemicals” Carcinogenesis 36: S2-S18.

  12. P. Moon, S. Penuela, K. Barr, C.L. Pin, I. Welch, M. Attur, S.B. Abramson, D.W. Laird* and F. Beier* (2015) “Cartilage-specific deletion of Panx3 prevents the development of surgically induced osteoarthritis” Journal of Molecular Medicine 93:845-856. *Co-senior authors.

  13. F. Molica, S. Morel, M.J. Meens, J.-F. Denis, P.F. Bradfield, S. Penuela, A. Zuffery, H. Monyer, B.A Imhof, M. Chanson, D.W. Laird, P. Fontana and B.R. Kwak (2015) “Functional role of a polymorphism in the pannexin1 gene in collagen-induced platelet aggregation” Thrombosis & Haemostasis 114: 1-12