Reto Asmis, PhD, Professor,
|Room:||300.21 - STRF|
|Education:||M.S. (Organic Chemistry), Ph.D. (Biochemistry), University of Fribourg, Switzerland|
|Post Doctoral:||University of California at San Diego, University of Berne, Switzerland|
|Cross Appointments:||Departments of Clinical Lab Sciences and Biochemistry|
|Other Faculty Positions:||Professor, Department of Clinical Lab Sciences|
Professor, Department of Radiology
Professor, Department of Biology, UTSA
MACROPHAGES, THIOL REDOX SIGNALING AND CHRONIC INFLAMMATORY DISEASES
Chronic inflammatory diseases are associated with monocyte and macrophage dysfunction. Our laboratory studies novel molecular signaling mechanisms involved in monocyte/macrophage dysfunction and their role in dysregulated inflammatory processes, including atherosclerosis and other complications associated with metabolic diseases such as diabetes. We found that dysfunctional macrophages not only show increased levels of ROS formation, but they also accumulate mixed disulfides between protein thiols (PSH) and glutathione (GSH), a process referred to as protein S-glutathionylation. We could show that several features associated with monocyte/macrophage dysfunction, including dysregulated cytokine release and enhanced chemotaxis are mimicked by healthy cells that were exposed to oxidants that promote protein-S-glutathionylation. Emerging evidence suggest that S-glutathionylation/deglutathionylation represents a novel, redox-based signaling paradigm similar to phosphorylation/dephosphorylation. Our preliminary evidence supports the hypothesis that only specific proteins are targeted for S-glutathionylation, and depending on the oxidative insult, selected signaling pathways are attenuated. Our data suggest that enhanced protein-S-glutathionylation is a common feature in monocytes and macrophages dysfunction, but that different environments may promote different S-glutathionylation patterns. The goal of our research is aimed at understanding the mechanisms leading to enhanced protein-S-glutathionylation and at identifying proteins and their signaling pathways targeted for S-glutathionylation.
Furthermore, we are interested in phytonutrients with anti-inflammatory properties that activate the cellular thiol antioxidant system and thus may protect monocytes against thiol oxidative stress and cell dysfunction. To this end, we are examining the effects of ursolic acid and its analogues on atherosclerosis and diabetic complications.
- Redox regulation of 14-3-3ζ controls monocyte migration.
Kim HS, Ullevig SL, Nguyen HN, Vanegas D, Asmis R
Arterioscler Thromb Vasc Biol: 2014-07-01; 34(7); 1514-21 Epub: 2014-05-08.
PMID: 24812321   LINK:
- Bioenergetic profiles diverge during macrophage polarization: implications for the interpretation of 18F-FDG PET imaging of atherosclerosis.
Tavakoli S, Zamora D, Ullevig S, Asmis R
J Nucl Med: 2013-09-01; 54(9); 1661-7 Epub: 2013-07-25.
PMID: 23886729   LINK:
- Reactive oxygen species and thiol redox signaling in the macrophage biology of atherosclerosis.
Tavakoli S, Asmis R
Antioxid Redox Signal: 2012-12-15; 17(12); 1785-95 Epub: 2012-06-11.
PMID: 22540532   LINK:
- Redox regulation of MAPK phosphatase 1 controls monocyte migration and macrophage recruitment.
Kim HS, Ullevig SL, Zamora D, Lee CF, Asmis R
Proc Natl Acad Sci U S A: 2012-10-09; 109(41); E2803-12 Epub: 2012-09-18.
PMID: 22991462   LINK:
- Nox4 is a novel inducible source of reactive oxygen species in monocytes and macrophages and mediates oxidized low density lipoprotein-induced macrophage death.
Lee CF, Qiao M, Schröder K, Zhao Q, Asmis R
Circ Res: 2010-05-14; 106(9); 1489-97 Epub: 2010-04-01.
PMID: 20360249   LINK:
Complete Publication Listing