Dr Ian McKay, BA DPhil

Lecturer

Contact Details:

Graduated from Oxford in 1988 with a degree in Pure and Applied Biology

DPhil in Oxford 1988-1992 at the Imperial Cancer Research Fund, Developmental Biology Unit supervised by Dr Julian Lewis.

Thesis focused on the development of the inner ear in normal and mutant mice.

1992 Moved to London as Post-doctoral Research Fellow for Professor Andrew Lumsden – head of MRC Developmental Neurobiology Unit at Guy’s Hospital

Studied focused on the patterning of cranial nerves.

1996 to present joined Barts and London School of Medicine and Dentistry

Since coming to Queen Mary’s I have worked on a range of projects including:

• Osteogenic Bioactive Materials

• Genetic Predisposition to Periodontal Disease

• Genes induced by bone morphogenetic proteins

• Risk factors for Periodontal disease

• Genetic polymorphisms and their role in drug-induced gingival overgrowth

Publications:

Bostanci, N., Allaker, R., Johansson U., Rangarajan, M., Curtis, M. A., Hughes, F.J. and McKay I.J. (2007). Interleukin-1α stimulation in monocytes by periodontal bacteria: antagonistic effects of Porphyromonas gingivalis Oral Microbiology and Immunology 22; 52-60.

Bostanci, N., Ilgenli, T., Emingil, G., Afacan, B., Han, B., Atilla, G., McKay, I.J., Hughes F.J. and Belibasakis, G.N. (2007). Differential expression of receptor activator of nuclear factor-kappaB ligand and osteoprotegerin mRNA in periodontal diseases. J Periodontal Res. 42; 287-93.

James, J.A., Poulton, K.V., Howarth, S.E., Payne, D., McKay, I.J., Hughes, F.J. and Linden, G.J. (2007). Polymorphisms of TLR4 but not CD14 are associated with a decreased risk of aggressive periodontitis. Journal of Clinical Periodontology 34; 111-117.

Allaker, R. P., Sheehan, B. E, McAnerney, M.C. and McKay, I. J. (2007). Interaction of adrenomedullin and calcitonin gene related peptide with the periodontal pathogen Porphyromonas gingivalis. FEMS Immunology & Medical Microbiology 49; 91-97.

Hussain, Q.A., Sheehan, B.E., McKay, I.J. and Allaker, R. P. (2007). Antimicrobial activity does not predict cytokine response to adrenomedulin. Mediators of Inflammation 2007 epub ref 30987

Bostanci, N, Allaker, R.P., Belibasakis, G.N., Rangarajan, M., Curtis, M.A., Hughes, F.J. and McKay, I.J. (2007). Porphyromonas gingivalis antagonises Campylobacter rectus induced cytokine production by human monocytes. Cytokine. 2007 39:147-56.

Hughes, F. J. Syed, M., Koshy, B., Marinho, V., Bostanci, N., McKay, I. J., Curtis, M.A., Croucher, R.E. and Marcenes, W. (2006). Prognostic factors in the treatment of generalised aggressive periodontitis: I. Clinical features and initial outcome. Journal of Clinical Periodontology 33; 663-670.

Hughes, F. J. Syed, M., Koshy, B., Bostanci, N., McKay, I. J., Curtis, M.A., Marcenes, W. and Croucher, R.E. (2006). Prognostic factors in the treatment of generalised aggressive periodontitis: II. Effects of smoking on initial outcome. Journal of Clinical Periodontology 33; 671-676.

Bostanci, N., Ilgenli, T., Can Pirhan, D., Clarke, F.M., Marcenes, W., Atilla, G., Hughes, F.J. and McKay, I. J. (2006). IL-1A gene polymorphisms are associated with altered risk of gingival overgrowth in renal transplant patients receiving Cyclosporin A Journal of Clinical Periodontology 33; 771-778.

Edgar, A.J., Dover, S.L., Lodrick, M.N., McKay, I.J., Hughes, F.J. and Turner, W. (2005). Bone morphogenetic protein-2 induces expression of murine zinc finger transcription factor ZNF450. J Cell Biochem. 94:202-15.

Petropoulos, G., McKay, I.J. and Hughes, F.J. (2004). The association between neutrophil numbers and interleukin-1 concentrations in the gingival crevicular fluid of smokers and non-smokers with periodontal disease. Journal of Clinical Periodontology 31;390-395

Sarmento, C., Luklinska, Z., Brown, L., Anseau, M., De Aza, P., De Aza, S., Hughes, F.J. and McKay, I.J. (2004). The in vitro behaviour of osteoblastic cells cultured in the presence of pseudowollastonite ceramic’. Journal of Biomedical Materials Research 69A; 351-358.

Dufane, D., Delloye, C., McKay, I.J., De Aza, P.N., De Aza, S., Schnieder, Y.J. and Anseau, M. (2003). Indirect cytotoxic evaluation of psuedowollastonite. J. Mater Sci: Mater Med 14; 33-38.

McGonnell, I. M, McKay, I.J. and Graham, A. (2001). The anatomical and evolutionary implications of a cranial neural crest contribution to the avian clavicle. Dev Biol 236; 354-363.

McKay, I.J. and Hughes F.J. (2000). Genetic tests mark new era for dentistry [letter].

Br Dent J. 188; 118.

Shirodaria, S., Smith, J., McKay, I.J., Kennett, C.N. and Hughes, F.J. (2000). Polymorphisms in the IL-1a gene are correlated with levels of interleukin-1a protein in the gingival crevicular fluid of teeth with severe periodontal disease. J. Dent. Res 79; 1864-1869.

Logan, C., Wingate, R.J.T., McKay, I.J. and Lumsden, A. (1998). Tlx1 and Tlx3 homeobox gene expression in cranial sensory ganglia and hindbrain of the chick embryo: markers of patterned connectivity. J. Neurosci. 18; 5389-5402.

McKay, I.J., Lewis, J. and Lumsden, A. (1997). The organisation and development of facial motor neurons in the kreisler mutant mouse. Eur. J. Neurosci. 9; 1499-1506.

McKay, I.J., Lewis, J. and Lumsden, A. (1996). The role of FGF-3 in early inner ear development: An analysis in normal and kreisler mutant mice. Dev. Biol. 174; 370-378.

Shimeld, S.M., McKay I.J. and Sharpe, P.T. (1996). The murine homeobox gene Msx-3 shows a highly restricted expression in the developing neural tube. Mech. Dev. 55; 201-210.

McKay,I.J., Muchamore, A., Krumlauf, R. Maden, M., Lumsden, A. and Lewis, J. (1994). The kreisler mouse: a hindbrain segmentation mutant that lacks two rhombomeres. Development 120; 2199-2111.

Research interests:

• Using proteomic approaches to identify markers of periodontal disease using proteomic methods

• Investigate the diversity of bone cell populations in the adult

• Testing the role that gingival connective tissues play in limiting the regeneration of alveolar bones

• Examining the response of the host cells and tissue to different oral bacteria and how these responses can be modulated by both bacteria and systemic treatments