Contact info

Dr Shao-Ling Zhang
CRCHUM � Pavillon R
900, Saint-Denis � Room R08-442
Montreal, QC H2X 0A9

Tel: 1-514-890-8000, ext. 15633
E-mail: [email protected]

Research keywords

Dr Zhang obtained her Bachelor of Medicine (1989) from Shanghai Medical University, China. Then, she obtained her MSc (1999) and PhD (2002, recipient of a CIHR doctoral award) degrees from the Universit� de Montr�al in the Department of Biomedical Sciences under the supervision of Dr John Chan (CRCHUM). With the support of a CIHR research fellowship (2002-2004), she finished her post-doctoral training at Massachusetts General Hospital at Harvard Medical School under the supervision of Dr Julie Ingelfinger. In October 2004, she was recruited back to CRCHUM and MDRC as an independent investigator. She was the recipient of Young Investigator Award from CIHR-KRESCEN (Kidney Research Scientist Core Education and National Training; 2005-2008) program and Chercheur-boursier junior I du FRSQ (2005-2009). Currently, she is a scholar of Chercheur-boursier junior II du FRSQ (2010-2013). With financial supports by the CIHR, Kidney Foundation of Canada, FRSQ, Fondation du CHUM, Leader Opportunity Fund of Canada Foundation for Innovation (CFI) and Heart Stroke Foundation of Quebec, her research program has been focused on the area of "Maternal Diabetes and Perinatal Programming of Kidney and Cardiovascular Diseases".

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As an adverse in utero environment, maternal diabetes appears to program offspring to the development of other problems later in life, such as hypertension, obesity and the cardiometabolic syndrome. This phenomenon, called perinatal programming, has attracted worldwide attention in recent decades, yet its mechanism(s) is incompletely understood. In the past 5 years, Dr Zhang's laboratory has carried out in vitro, ex vivo and in vivo studies to investigate this phenomenon. By manipulating the levels of maternal hyperglycemia in pregnant mice, the obtained offspring have displayed 2 distinct phenotypes: microsomic offspring from severe maternal diabetes, and macrosomic offspring from diabetic dams with insulin treatment. Microsomic offspring have relatively small neonatal kidneys with ~40% fewer nephrons. In contrast, macrosomic offspring have apparently normal neonatal kidney size. Offspring from diabetic dams manifest hypertension, glucose intolerance and kidney injury in adulthood as well as heightened intrarenal reactive oxygen species (ROS) generation, sodium re-absorption and renin-angiotensin system (RAS) activation with down-regulation of angiotensin-converting enzyme 2 (ACE2) expression. Moreover, hyperglycemia-induced nascent nephron apoptosis occurs, likely accounting for the low nephron number. This nascent nephron apoptosis is mediated, at least in part, via ROS generation and activation of the transcriptional nuclear factor-kappa B (NF-κB) and p53 pathways.

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Current ongoing projects in the laboratory:

Role of reactive oxygen species (ROS) in maternal diabetes-induced perinatal programming. The aim is to establish the crucial role of intrarenal ROS in mediating maternal diabetes-induced dysnephrogenesis and perinatal programming of hypertension and kidney injury and to delineate the underlying mechanisms of ROS action.

Role of Angiotensin Converting Enzyme-2 (ACE2) gene expression on maternal diabetes-induced perinatal programming of hypertension. The aim is to establish the crucial role of intrarenal ROS impact on ACE2 gene expression on maternal diabetes-induced dysnephrogenesis and perinatal programming of hypertension and kidney injury and to delineate the underlying mechanisms.