LHI Lectures

2009-2010 LHI Lecture Series

Every Wednesday, Noon - 1pm
3-100 Mayo Auditorium - campus location / room location

download schedule (pdf format, requires free Acrobat Reader)
Schedule is subject to change; check back for updates!

 LHI Lecture September 30, 2009
Transcriptional regulation of cardiac morphogenesis
Daniel J. Gary, MD, PhD
Professor of Medicine and St. Jude Medical Endowed Chair in Cardiology
Director, Lillehei Heart Institute
Chief, Cardiovascular Division
University of Minnesota Medical School
» more info about Dr. Garry from the Cardiovascular Division web site

Lecture webcast recording

 LHI Lecture October 7, 2009
The Regulation of Central Angiotensin Receptor Expression in Heart Failure and its Role in Sympatho-Excitation
Irving H. Zucker, Ph.D.
Theodore F. Hubbard Professor of Cardiovascular Research
Chairman, Department of Cellular & Integrative Physiology
University of Nebraska Medical Center
» more info about Dr. Zucker from the Cardiovascular Division web site

Lecture webcast recording

Abstract:
A variety of peripheral and central mechanisms contribute to the progressive deterioration of cardiovascular regulation in the setting of chronic heart failure (CHF). Increased sympathetic outflow increases myocardial oxygen consumption, peripheral resistance and activates the renin-angiotensin system. It is important to understand the molecular and cellular mechanisms that are responsible for the sympatho-excitatory process in CHF. This seminar will focus on studies designed to understand the roles of Angiotensin II (Ang II), angiotensin receptors, and reactive oxidant stress on sympathetic activation in animal models of CHF. The data presented willdemonstrate that CHF is accompanied by an increase in Ang II in the central nervous system along with a significant up regulation of the Angiotensin Type 1 receptor (AT₁R), a decrease in the AT₂R. Furthermore, Angiotensin Converting Enzyme (ACE) is increased while its catabolic homologue, ACE₂ is decreased in areas of the medulla that regulate sympathetic outflow. The increase in AT₁R expression is mediated by activation of at least two transcription factors, Activator Protein-1 (AP-1) and Nuclear Factor Kappa B (NF_ΚB). The up regulation of AT₁R expression is dependent on Ang II binding thus initiating a positive feedback system further increasing sympathetic outflow. Activation of the AT₁R initiates an NADPH oxidase dependent increase in superoxide anion. Superoxide reduces the bioavailability of nitric oxide and thereby promotes the formation of peroxynitrite which nitrosylates a variety of proteins that regulate ion channel function. Superoxide also activates transcription factors that are involved with the regulation of Ang II receptor expression. All of the above processes contribute to a process of sympatho-excitation in CHF that promotes a downward spiral of cardiovascular deterioration.

 LHI Lecture October 14, 2009
The Regulation of Central Angiotensin Receptor Expression in Heart Failure and its Role in Sympatho-Excitation
Joseph M. Metzger, Ph.D.
Professor & Chair, Department of Integrative Biology & Physiology
Maurice B. Visscher Endowed Chair in Physiology
University of Minnesota Medical School
» more info about Dr. Metzger from the IGP web site

Lecture webcast recording

 LHI Lecture October 28, 2009
The Regulation of Central Angiotensin Receptor Expression in Heart Failure and its Role in Sympatho-Excitation
Vivian J. Bardwell, Ph.D.
Associate Professor
Department of Genetics, Cell Biology and Development/Cancer Center
University of Minnesota Medical School
» more info about Dr. Bardwell from the GCBD web site

Lecture webcast recording

Abstract:
The transcriptional corepressor BCOR regulates gene expression in association with a complex of proteins capable of epigenetic chromatin modification. Mutations in human BCOR result in the X-linked Oculofaciocardiodental (OFCD) syndrome that involves developmental defects in multiple systems, including the ocular, skeletal, and cardiovascular systems. To determine the role of Bcor in mouse development, we have generated Bcor loss-of-function alleles in embryonic stem (ES) cells and in mice. In vitro differentiation of ES cells harboring Bcor loss-of-function alleles demonstrated a role for Bcor in the regulation of gene expression very early in ES cell differentiation into ectoderm, mesoderm, and downstream hematopoietic lineages. To unravel Bcor’s complex role during early embryogenesis and specifically in cardiovascular development, we are currently generating ubiquitous and cardiac-specific Bcor knockout mice. Initial findings reveal that ubiquitous Bcor inactivation in mice results in male lethality prior to embryonic turning and late gestation lethality of heterozygous females. Meanwhile, Bcor inactivation in males in the neural crest cell lineage results in perinatal lethality possibly due to observed cardiovascular defects.