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- Catriona Kelly
I completed my BSc in Biomedical Sciences at the University of Ulster, Coleraine in 2004. I subsequently undertook a PhD at the University of Ulster which examined the role of cellular communication in insulin secretion and developed a pseudoislet model to study the importance of gap junction mediated cell-to-cell contact in normal beta-cell function. In 2007, I began my post-doctoral career at Queen’s University of Belfast where I first worked on the molecular mechanisms involved in the regulation of retinal perfusion and blood pressure and the pathophysiological changes responsible for the disruption of retinal blood flow during early diabetes. I consequently moved onto to study NF-kB driven inflammation in the airways epithelium and the molecular mechanisms leading to dysfunction of these signalling pathways in inflammatory lung diseases such as Asthma and Cystic Fibrosis. I joined Keele as a Lecturer in Bioscience in February 2011.
ISTM research theme: Clinical & Diagnostic Science
My research interests are in inflammatory lung diseases such as Cystic Fibrosis and asthma and in particular, the molecular defects that lead to uncontrolled inflammation in these diseases. The work seeks to identify novel genetic predictors of inflammation in chronic airways disease at the earliest possible stage in an attempt to predict disease development and inform treatment regimes. A primary focus of the work is how the regulation of the NF-kB pathway is altered and how this contributes to disease progression and severity.
Kelly C, Canning P, Buchanan PJ, Williams MT, Elborn JS, Ennis M, Schock BC. (2013.) TLR4 is not targeted to the lysosome in Cystic Fibrosis. AJP: Lung, In Press
Kelly C, Williams MT, Mitchell K, Elborn JS, Ennis M, Schock BC. (2012) Expression of the NF-κB inhibitor A20 is altered in the Cystic Fibrosis epithelium. Eur Respir J. E-Pub Sept 2012
Kelly C, Williams MT, Elborn JS, Ennis M, Schock BC. (2012) Expression of the inflammatory regulator A20 correlates with lung function in patients with cystic fibrosis. J Cyst Fibros. E-Pub Nov 2012.
Abed A, Critchlow C, Flatt PR, McClenaghan NH, Kelly C. (2012). Directed differentiation of progenitor cells towards an islet-cell phenotype. Am J Stem Cell. 1(3):196-204
Guo-Parke H, McCluskey JT, Kelly C, Hamid M, McClenaghan NH, Flatt PR. (2012). Configuration of electrofusion-derived human insulin-secreting cell line as pseudoislets enhances functionality and therapeutic utility. J Endocrinol. 214(3):257-65.
Kelly C, Flatt CC, McClenaghan NH. (2011) Stem cell-based approaches for the treatment of diabetes. Stem Cells Int. Epub 2011 May 18.
Kelly C, McClenaghan NH, Flatt PR. (2011). Role of islet structure and cellular interactions in the control of insulin secretion. Islets. 3(2):41-7.
Kelly C, Shields MD, Elborn JS, SchockBC. (2011). A20 regulation of nuclear factor-κB: perspectives for inflammatory lung disease. Am J Respir Cell Mol Biol. 44(6):743-8.
Persaud SJ, Arden C, Bergsten P, Bone AJ, Brown J, Dunmore S, Harrison M, Hauge-Evans A, Kelly C, King A, Maffucci T, Marriott CE, McClenaghan N, Morgan NG, Reers C, Russell MA, Turner MD, Willoughby E, Younis MY, Zhi ZL, Jones PM. (2010). Pseudoislets as primary islet replacements for research: report on a symposium at King's College London, LondonUK. Islets. 2(4):236-9.
Kelly C, Parke HG, McCluskey JT, Flatt PR, McClenaghan NH. (2010). The role of glucagon- and somatostatin-secreting cells in the regulation of insulin release and beta-cell function in heterotypic pseudoislets.Diabetes Metab Res Rev.26(7):525-33.
Kelly C, Flatt PR, McClenaghan NH. (2010). Cell-to-cell communication and cellular environment alter the somatostatin status of delta cells. Biochem Biophys Res Commun. 399(2):162-6.
Kelly C, Guo H, McCluskey JT, Flatt PR, McClenaghan NH. (2010). Comparison of insulinrelease from MIN6 pseudoislets and pancreatic islets of Langerhans reveals importance of homotypic cell interactions. Pancreas. 39(7):1016-23.
Selected Publications
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Toll Like Receptor 4 is not targeted to the lysosome in Cystic Fibrosis airway epithelial cells. American Journal of Physiology: Lung Cellular and Molecular Physiology. doi>
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Expression of the NF-kappaB inhibitor A20 is altered in the Cystic fibrosis epithelium. European Respiratory Journal. doi>
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2012. CF AIRWAY EPITHELIAL CELLS LACK THE ANTI-INFLAMMATORY DOMAIN OF THE NF-KB INHIBITOR A20. PEDIATRIC PULMONOLOGY (vol. 47, p. 274). link>
Full Publications List show
Journal Articles
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Toll Like Receptor 4 is not targeted to the lysosome in Cystic Fibrosis airway epithelial cells. American Journal of Physiology: Lung Cellular and Molecular Physiology. doi>
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Expression of the NF-kappaB inhibitor A20 is altered in the Cystic fibrosis epithelium. European Respiratory Journal. doi>
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2012. INVESTIGATING THE ROLE OF THE PANCREATIC BETA-CELL IN THE DEVELOPMENT OF CF-RELATED DIABETES USING PSEUDOISLET MODELS. PEDIATRIC PULMONOLOGY, vol. 47, 283. link>
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2012. Directed differentiation of progenitor cells towards an islet-cell phenotype. Am J Stem Cells, vol. 1(3), 196-204. link>
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2011. CF EPITHELIAL CELLS LACK THE ZINC FINGER DOMAIN OF A20 AND THEREFORE CANNOT TERMINATE NF-KB SIGNALLING. PEDIATRIC PULMONOLOGY, 262. link>
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2010. The role of glucagon- and somatostatin-secreting cells in the regulation of insulin release and beta-cell function in heterotypic pseudoislets. Diabetes/Metabolism Research and Reviews, vol. 26(7), 525-533. doi>
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2009. INHIBITION OF A20 SIGNALLING IN CYSTIC FIBROSIS EPITHELIUM. PEDIATRIC PULMONOLOGY, 232. link>
Other
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2012. CF AIRWAY EPITHELIAL CELLS LACK THE ANTI-INFLAMMATORY DOMAIN OF THE NF-KB INHIBITOR A20. PEDIATRIC PULMONOLOGY (vol. 47, p. 274). link>
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2012. ROLE OF INHIBITOR OF APOPTOSIS (IAP) IN CF AIRWAY INFLAMMATION - MODIFICATION BY SMAC MIMETICS. PEDIATRIC PULMONOLOGY (vol. 47, p. 270). link>
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2011. ALTERED EXPRESSION OF THE NF-kappa B INHIBITOR A20 REFLECTS CFTR MUTATION AND FEV1. PEDIATRIC PULMONOLOGY (p. 259). link>
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2010. A20 REGULATION OF INFLAMMATION IN THE CYSTIC FIBROSIS EPITHELIUM. PEDIATRIC PULMONOLOGY (pp. 269-270). link>
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2010. THE ROLE OF ENDO-LYSOSOMAL DEGRADATION IN TOLL-LIKE RECEPTOR DRIVEN INFLAMMATION IN THE CF EPITHELIUM. PEDIATRIC PULMONOLOGY (pp. 272-273). link>
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2010. TOLL-LIKE RECEPTOR EXPRESSION AND ITS REGULATION BY CFTR. PEDIATRIC PULMONOLOGY (pp. 263-264). link>
Module 2 PBL Tutor for Keele MBChB Medical Degree.

