Contact info

Dr John S.D. Chan
CRCHUM � Pavillon R
900, Saint Denis - Room R08.448

Tel: 1-514-890-8000, ext. 15080
Fax: 1-514-412-7204
E-mail: [email protected]

Research keywords

John Chan was trained in Physiology and Biochemistry at the University of Manitoba, where he obtained a PhD degree under the supervision of Dr Henry G. Friesen. His thesis was in the field of Endocrinology. He then worked as a post-doctoral fellow on �Biosynthesis and secretion of pro-opiomelanocortin in human pituitary� in the laboratory of Dr Michel Chr�tien at the Institut de Recherches Cliniques de Montr�al and the laboratory of Dr Dorothy Krieger (deceased) of Mount Sinai Medical Centre, New York, NY. He then returned to Montreal and worked at the Institut de Recherches Cliniques de Montr�al as a Research Associate and then promoted as a Research Assistant Professor in the Department of Physiology, University of Montreal. He later worked as a Visiting Scientist and Visiting Assistant Professor at the National Institutes of Health (NIH) of USA and Harvard Medical School, respectively. Finally, he returned back to Montreal and worked as a Director of the laboratory of Molecular Nephrology and Endocrinology, Research Centre, Maisonneuve Rosemont Hospital of Montreal.

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As an independent investigator, Dr Chan demonstrated the presence of renin-angiotensin system in the kidney. He showed the expression of angiotensinogen (the sole precursor of the RAS) gene is under the regulation of catecholamines (sympathetic nervous system), implicating that intrarenal RAS activation may play an important role in hypertension development.

More recently, Dr Chan demonstrated that high glucose regulates angiotensinogen gene expression in the kidney via reactive oxygen species generation. By employing transgenic mouse models, Dr Chan�s group demonstrated unequivocally that overexpression of angiotensinogen specifically in the kidney induces hypertension, albuminuria and kidney injury. In contrast, overexpression of catalase specifically in the kidney attenuates RAS activation, hypertension, albuminuria and kidney cell apoptosis in diabetes.

Finally, in collaboration with the groups of Dr Catharine Whiteside and Dr George I. Fantus, Dr Chan has identified several genes that are differentially up-regulated in diabetic kidneys and they might play an important role in tubular apoptosis and atrophy in diabetes.

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The role of intrarenal RAS and ROS in the pathogenesis of diabetic nephropathy, with special emphasis on renal angiotensinogen gene expression and intrarenal ROS generation on tubular apoptosis in diabetes. Transgenic mice specifically overexpressing angiotensinogen and catalase in the kidney will be used to study the molecular mechanism(s) of intrarenal RAS and ROS action on the induction of tubular fibrosis and apoptosis in diabetes. Gene chip microarrays will be used to identify the unique genes that are differentially expressed in diabetic kidneys. The physiological role(s) of these unique genes will be studied in vitro and in vivo.