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.
- Monocytic MKP-1 is a Sensor of the Metabolic Environment and Regulates Function and Phenotypic Fate of Monocyte-Derived Macrophages in Atherosclerosis.
Kim HS, Tavakoli S, Piefer LA, Nguyen HN, Asmis R
Sci Rep: 2016-09-27; 6(); 34223 Epub: 2016-09-27.
PMID: 27670844   LINK:
- Monocytes and Macrophages: A Fresh Look at Functional and Phenotypic Diversity.
Antioxid Redox Signal: 2016-09-07; (); Epub: 2016-09-07.
PMID: 27488399   LINK:
- Protein Thiol Redox Signaling in Monocytes and Macrophages.
Short JD, Downs K, Tavakoli S, Asmis R
Antioxid Redox Signal: 2016-07-13; (); Epub: 2016-07-13.
PMID: 27288099   LINK:
- Protein S-Glutathionylation Mediates Macrophage Responses to Metabolic Cues from the Extracellular Environment.
Ullevig SL, Kim HS, Short JD, Tavakoli S, Weintraub ST, Downs K, Asmis R
Antioxid Redox Signal: 2016-05-17; (); Epub: 2016-05-17.
PMID: 26984580   LINK:
- Glutaredoxin 2a overexpression in macrophages promotes mitochondrial dysfunction but has little or no effect on atherogenesis in LDL-receptor null mice.
Zamora DA, Downs KP, Ullevig SL, Tavakoli S, Kim HS, Qiao M, Greaves DR, Asmis R
Atherosclerosis: 2015-07-01; 241(1); 69-78 Epub: 2015-04-26.
PMID: 25966442   LINK:
Complete Publication Listing