Dr Philip Padfield BSc (Hons), PhD
Senior Lecturer
- Email: Philip.V.Padfield@manchester.ac.uk
- Telephone: +44 (0)161 275 1820
Epithelial Sciences Research Group
School of Tanslational Medicine
Stopford Building
Oxford Road
Manchester, M13 9PT
Memberships of Committees and Professional Bodies
Biochemical Society (UK)
Nutrition Society (UK)
Research
My current research interests are centred on improving our limited understanding of how indiviudal components of the human diet modify the internal biochemistry of the body's cells to either promote health and well being or faciliate the progression of disease. Resaerch project currently ongoing in my lab include:
1) Can diet modify of the profile of eicosanoid synthesis? This project employs a nutriomic based systems approach to expand our understanding of how dietary polyunsaturated fatty acids (PUFAs) influence the profile of eicosanoid synthesis elicited by an inflammatory stimulus. The primary aim of the project is use in experimental data generated in vitro to develop a new dynamic flux model of eicosanoid synthesis. This will be used to examine in silico how dietary supplementation with arachidonic acid, eicosapentaenoic acid and docosahexaenoic acid influences the PUFA content of cell lipids and the expression of the individual enzymes components of the eicosanoid biosynthetic machinery, and how these changes influence the pattern of eicosanoids generated by an inflammatory stimulus.
2) Does the fatty acid content of the diet alter the inflammatory phenotype of the colonic mucosa? We are investigating how the fatty acid content of the diet, specifically the relative concentrations of saturated fatty acids, omega-3 PUFAs and omega-6 PUFAs, influence the transcriptome and proteome of colonic epiithelial cells, and how any changes impact the inflammatory phenotype of the colonic epithelium.
Methodological Knowledge
Over the past 25 years I've amassed a detailed knowledge and expertise in many areas of cell biology and biochemistry, including the use of biochemical and morphological based assays to explore the molecular requiremenst of vesicle mediated protein transport, protein-protein interactions and intracellular signalling. Techniques that have been, or are being, routienaly used in my laboratory include: isolation and primary culture of colonic epithelail cells and pancreatic acinar cells, culture of assorted immortalised epithelial cell lines, subcellular fractionation, fatty acid anlysi by TLC and GC, protein isolation and purification by LC and HPLC, western blot analysis, immunoprecipitation and various assays for enzyme activity.
Teaching
Programme Director MSc/Dip in Clinical Biochemistry
Programme Director PG Certificate in Research Methods in Translational Medicine
Programme Director MRes in Tanslational Medicine
Postgraduate Teaching Director for School of Translational Medicine
Biography
1999 - Present Senior Lecturer, School Translataional Medicine, University of Manchester, UK
1993 – 1999 Assistant Professor, Departments of Internal Medicine and Pathology, St. Louis university, St. Louis, MO USA
1990 – 1993 Assistant Research Scientist, Department of Cell Biology, Yale University, CT USA
1988 – 1990 Postdoctoral Associate, Department of Cell Biology, Yale University, CT USA
Qualifications
BSc (Hons) Biochemistry, University of Bristol, UK
PhD (Physiology), University of Manchester, UK
Collaborators and affiliated staff
Collaborators
Dr Cath O'Neill, School of Translational Medicine, University of Manchester
Dr John McLaughlin, School of Translational Medicine, University of Manchester
Prof Anna Nicoloau, School of Life Sciences, University of Bradford
Dr Stephen Wilkinson, Dept. Chemical and Process Engineering, University of Sheffield
Publications
2009
- McLaughlin J., Lambert D., Padfield P.J., Burt J.P. & O'Neill CA. (2009). The mycotoxin patulin, modulates tight junctions in caco-2 cells. Toxicology In Vitro, 23, 83-88. eScholarID:133517 | DOI:10.1016/j.tiv.2008.10.009
- McLaughlin JT, Lambert DS, Padfield PJ, Julian PH Burt, O'Neill CA. (2009). The mycotoxin Patulin, modulates tight junctions in Caco-2 cells. Toxicology in vitro, 23, 83-88. eScholarID:1d28295 | DOI:10.1016/j.tiv.2008.10.009
2007
- Duraisamy Y, Lambert DS, O'Neill CA, Padfield PJ. (2007). Differential incorporation of docosahexaenoic acid into distinct cholesterol-rich membrane raft domains. Biochemical and Biophysical Research Communications, 360, 886-890. eScholarID:1d27861
- Lambert DS, O'Neill CA, Padfield PJ. (2007). Methyl-beta-cyclodextrin increases permeability of Caco-2 cell monolayers by displacing specific claudins from cholesterol rich domains associated with tight junctions. Cellular Physiology and Biochemistry, 20, 495-506. eScholarID:1d27859
- Lambert DS, Padfield PJ, McLaughlin JT, Cannell S, O'Neill CA. (2007). Ochratoxin A displaces claudins from detergent resistant membrane microdomains. Biochem. Biophys. Res. Commun, 358(2), 632-636. eScholarID:1d27725 | DOI:10.1016/j.bbrc.2007.04.180
2006
- Visanji JM, Thompson DG, Padfield PJ. (2006). Induction of G2/M phase cell cycle arrest by carnosol and carnosic acid is associated with alteration of cyclin A and cyclin B1 levels. Cancer Letters, 237, 130-136. eScholarID:1d26493
2005
- Lambert D. O'Neill C.A. Padfield, P.J. (2005). Depletion of Caco-2 Cell Cholesterol Disrupts Barrier Function by Altering the Detergent Solubility and Distribution of Specific Tight Junction Proteins. Biochemical Journal, 387, 553-560. eScholarID:9432
2004
- Lambert DS, O'Neill CA, Padfield PJ. (2004). Depletion of caco-2 cell cholesterol disrupts barrier function by altering the detergent solubility and distribution of specific tight junction proteins. Biochemical Journal, 387 (Pt2), 553-60. eScholarID:1d26156 | DOI:10.1042/BJ20041377
- McLaughlin JT, Padfield PJ, JP Burt, O'Neill CA. (2004). Ochratoxin A increases permeability through tight junction removal of specific claudin isoforms. Amer. J. Physiol-cell physiol, 287(5), 1412-1417. eScholarID:1d25860 | DOI:10.1152/ajpcell.00007.2004
- Visanji JM, SJ Duthie, L Pirie, Thompson DG, Padfield PJ. (2004). Dietary isothiocyanates inhibit Caco-2 cell proliferation and induce G2/M phase cell cycle arrest, DNA damage, and G2/M checkpoint activation. Journal Of Nutrition, 134, 3121-3126. eScholarID:1d26064