Contact info

Dr Pedro M. Geraldes
3001, 12^e Ave North
Sherbooke, QC J1H 5N4

Tel: 1-819-820-6868, ext. 12442
Fax: 1-819-564-5292
E-mail: [email protected]

Link to Geraldes Lab webpage

Research keywords

Pedro Geraldes was trained in Biochemistry at the University of Montreal where he obtained a PhD degree. He studied the role of hormone receptors during vascular healing after percutaneous coronary intervention under the supervision of Dr J.-F. Tanguay. He then joined the laboratory of Prof. George L. King at Joslin Diabetes Center in Boston, where he worked as a post-doctoral fellow on PKC actions and vascular complications such as retinopathy, nephropathy and atherosclerosis. He recently joined the Department of Medicine at the University of Sherbrooke as an Assistant Professor.

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Diabetic patients are prone to increase macrovascular diseases such as atherosclerosis and microvascular complications such as neuropathy, nephropathy and retinopathy. Metabolite abnormalities induced by the lack of insulin, such as hyperglycemia and dyslipidemia, are believed to be the major risk factors for their development. However, much less studied is the importance of the response of local vascular tissues to the elevated levels of systemic glucose and lipid-induced toxic factors. For example, several clinical observations showed that the expression of VEGF is increased in the retina and kidney but decreased in the myocardium of diabetic animals and patients. These clinical results strongly supported the notion that vascular tissue react differently to adverse effects of hyperglycemia and other systemic toxic factors induced by diabetes. Identification of new mechanisms causing chronic vascular damage is still a challenge for on-going research on diabetic complications. Dr Geraldes recently demonstrated that the expression of SHP-1, a protein tyrosine phosphatase (PTP) that is critical in de-activating PDGF action, is elevated by diabetes and hyperglycemia in the retina, kidney and ischemic muscles. Increase expression of SHP-1 may cause vascular complication in the kidney (epithelial and endothelial cell death and dysfunction) and reduce collateral vessel formation during ischemia (diminution of oxygen to the tissue). The research projects of Dr Geraldes are related to study the mechanisms underlying hyperglycemia and lipid-induced protein kinase C (PKC) activation in the abnormalities of growth factor actions such as PDGF, VEGF, angiopoietin and insulin related to kidney, peripheral vessels and atherosclerotic plaque formation. Thus, finding new cellular targets involved in growth factor resistance and which are activated downstream by various toxic metabolites of glucose and lipids is crucial to identifying early markers of vascular diseases and new therapeutic targets in order to improve even reverse vascular complications of diabetic patients

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Current projects in the laboratory:

Inhibition of survival factors in diabetic nephropathy. Understanding how hyperglycemia-induced toxic metabolites that will contribute to podocyte and renal endothelial cell apoptosis and dysfunction leading to diabetic nephropathy. We are studying the mechanisms related to growth factor (VEGF, Angiopoietin) disorder and signaling pathway induced by angiotensin, glucose and lipid metabolism.

Mechanism for poor collateral vessel formation in diabetes. We are investigating the role of protein tyrosine phosphatase induced by hyperglycemia causing inhibition of growth factors actions (PDGF, VEGF, insulin) and poor collateral vessel formation during ischemia.

Protein kinase C and atherosclerotic plaque formation. The goal is to identify new target genes and potential markers regulated by protein kinase C activation and lipid metabolism involved in the atherosclerotic plaque formation in diabetes.

Our laboratory investigates these multiple factorial complications of the vessels using sophisticated animal models (Cre-lox/Tet-ON system) for tissue specific knock-down and the most recent molecular and cellular technologies including gene silencing (siRNA, shRNA), laser capture microscopy, biochemical and cellular assays.