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HEINRICH LOB

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About Heinrich

Hometown:
Erlenbach am Main, Germany

Education:
PHD, University of Cologne

Hobbies:
Music, darts, running, football (soccer)

Contact Info:

Email:
hel27@cornell.edu

Phone: 607-253-3677
Fax: 607-253-3378

Curriculum Vitae

 

Return to Lab Members

 

HeinrichLobpic

After I received my diploma in biology (Major: Biochemistry) at the University of Cologne in 2002, I began my doctorate at the Department of Pharmacology in Cologne, Germany.  My thesis dealt with beneficial effects of Ca2+ -channel agonists on endothelial cells under pathophysiological conditions.  An important part of the thesis was performed at Monash University in Melbourne, Australia in the laboratory of Grant Drummond. In 2006, I defended successfully and moved to Atlanta, Georgia to join David Harrison's laboratory at Emory University as a postdoctoral fellow and was later promoted into a faculty rank as Instructor.

Untypically for a vascular biology laboratory, I worked in my first year with mice which develop Acute Respiratory Distress Syndrome (ARDS) due to the acute loss of the extracellular dismutase (SOD3). These studies showed that pulmonary SOD3 is important to prevent increases in superoxide which leads to severe inflammation in the lungs. My main project however, was to identify the region in the body where reactive oxygen species (ROS) and especially superoxide are most important in the genesis of hypertension. In the first part of this study, I acutely deleted SOD3 in the circumventricular organs in the brain using adenoviral delivery of Cre-recombinase.  These mice developed moderate hypertension on baseline and after delivery of low-dose angiotensin II (140 ng/kg/min) severe hypertension.  Additionally, these mice developed severe peripheral inflammation and showed increased sympathetic activity compared to control mice. The second part focused on the vasculature.  In order to investigate if vascular ROS are important in the genesis of hypertension I created mice in which I deleted SOD3 specifically in the vascular smooth muscle cells.  To our surprise, these mice did not develop hypertension nor showed they had any sign of peripheral inflammation, despite observed increases in vascular superoxide.

In July 2011, I joined the Davisson Laboratory and will increase my knowledge about central control of blood pressure regulation, obesity and central regulation of inflammation.

 

Last update 2 August 2011
College of Veterinary Medicine - Ithaca, New York 14853-6401
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