Roles
Professor of Medicine
ACOS/Research MVAHS
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Biography
Robert M. Jackson is Professor of Medicine in the Division of Pulmonary and Critical Care Medicine and Associate Chief of Staff for Research at the Miami VAHS. He has a broad background in respiratory physiology and disease with specific training and expertise in both basic laboratory and clinical research. His present research focuses on mechanisms of exercise limitation (other than hypoxemia) in patients with idiopathic pulmonary fibrosis (IPF) and other interstitial lung diseases (ILD). As a funded VA investigator throughout my career, he has focused serially on mechanisms of adaptation to oxidant stress, the role of hypoxia in oxidative injury, and most recently on oxidative stress and fibrosis in IPF. His research group has developed strong ties with basic scientists who have expertise in intracellular signaling and mitochondrial function, and we have established ties with community pulmonologists for referrals and industry for clinical trial support. He has successfully, as demonstrated by peer-reviewed publications and grant funding from the NIH, VA, American Lung Association and American Heart Association and other agencies, administered complex research programs. Because of this background and experience, he is uniquely qualified to investigate basic mechanisms that underlie clinical problems that are clear risks for VA patients with lung disease or Gulf War Illness. This background is strengthened by organizational and administrative experience including creation of the IPF research and clinical programs at the University of Alabama at Birmingham (UAB) in the late 1990’s and his current role as director of the research program at the Miami VAHS. -
Education & Training
Education
Post Graduate Training
Licensures and Certifications
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Honors & Awards
No result found
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Teaching Interests
Every month, I teach residents and pulmonary fellows during rounds and in clinics. Yearly, I present formal lectures on ILD to second year medical students and physiology lectures to pulmonary fellows. I have served on a number of Masters and Doctoral thesis committees and formally advised degree candidates. In addition, I am a NAUI certified SCUBA and Nitrox Instructor teaching skills useful in scientific diving. -
Research Interests
My early publications directly addressed the mechanisms by which organisms, cells and organelles adapted to oxidant stress and overcame oxidative injury. These studies used often overlooked models of adaptation to stress to understand underlying mechanisms that led to survival in ozone, hyperoxia and during reoxygenation after hypoxia. Specifically, we found that hypoxia often down regulated cellular antioxidant defense mechanisms, while adaptation to oxidative stress was attributable to an up regulation of cellular antioxidant defenses. These basic studies led directly to the mechanisms of lung hypoxia-reoxygenation injury in mammals. Evidence derived from these studies has led (in part through an associated NIH RFA) to recognition of the clinical importance of lung hypoxia-reoxygenation injury, especially after trauma or lung transplantation.
I worked extensively with collaborators to elucidate how lung metabolic functions responded to acute and chronic hypoxia, focusing on the renin-angiotensin-aldosterone system and modulation of atrial natriuretic peptide (ANP). These studies built on observations that the lung vascular endothelium was metabolically active (e.g., converting angiotensin 1 to angiotensin 2) and that hypoxia and/or oxidative stress might impair normal endothelial homeostasis. These studies emphasized lung vascular function in isolated, perfused lungs in which we could assess peptide and lipid metabolism and precisely identify the role of ANP in regulation of pulmonary vascular resistance in hypoxia. These studies have proved durably relevant to patients with IPF, in whom pulmonary artery hypertension is common and brain natriuretic peptide has been shown by us to be elevated and to increase with exercise and accompanying hypoxemia.
The subsequent phase of my preclinical investigations focused on cellular mechanisms that regulate antioxidant defenses during hypoxia and reoxygenation. These basic studies are directly related to the proposed experiments that would elucidate how muscle tissue hypoxia (resulting from exercise-induced hypoxemia) and resulting oxidative stress limit the ability of patients with IPF and other ILD to exercise. In vitro cellular models including primary isolates of alveolar type 2 epithelial cells and related cell lines showed clearly that both hypoxia and oxidative stress modulated mitochondrial superoxide dismutase (MnSOD) and further revealed mechanisms (e.g., oxidative inhibition of Complex I) that impaired mitochondrial respiration. -
Publications
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Copyrights & Patents