Normand Leblanc Ph.D.

Professor

Cellular and Molecular Pharmacology & Physiology | Department of Pharmacology

Normand Leblanc

Contact Normand Leblanc Ph.D.

Location

Savitt Medical Science (SMS)
Room 50

1664 North Virginia Street
Savitt Medical Science
RenoNV 89557
Normand Leblanc

Education

  • B.S.B, 1981, University of Sherbrooke, Biophysics
  • M.S.B., 1983, University of Sherbrooke, Biophysics
  • Ph.D., 1987, University of Sherbrooke, Biology

Biography

Role of ion channels in the regulation of excitation-contraction coupling of cardiac and vascular smooth muscle cells in health and disease.

My laboratory is interested in determining the properties and function of ion channels and electrogenic ion transport systems in the control of vascular tone and cardiac excitation-contraction coupling. Using a wide array of electrophysiological (classical intracellular recording and patch clamp techniques), quantitative fluorescence imaging (Indo-1, Fura-2 and Fluo-4 epifluorescence and total internal reflection fluorescence microscopy or TIRFM) and biochemical (immunocytochemistry, Western Blot, enzyme assays) and molecular biological (cloning and expression of ion channel proteins) techniques, our efforts have mainly focused on investigating the biophysical properties and signaling pathways involved in the regulation of Ca2+-activated Cl- channels (CaCCs) in vascular smooth muscle cells. Recently, three independent groups of investigators have identified Tmem16a as the gene encoding for CaCCs in vascular myocytes. We are currently exploring how the protein encoded by this gene called TMEM16A or Anoctamin-1 is regulated by phosphorylation, and establish the identity of the kinases and phosphatases that are responsible for this process. Finally we recently found that the activity of CaCCs and expression of TMEM16A are up regulated in pulmonary artery smooth muscle cells from animal models of pulmonary hypertension and have embarked on studies examining the effect this increase activity has in the enhanced vasoconstriction and pulmonary arterial wall remodeling that are known to occur in human pulmonary arterial hypertension.