Reto Asmis, PhD photo
Reto Asmis, PhD

Reto Asmis, PhD, Professor & Associate Dean (GSBS)

Room:292.4-STRF
Phone:562-4054
Email:asmis@uthscsa.edu
Web Page(s):Asmis Lab
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

Research Interest:


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. We currently focus on four major projects:

1. Glutaredoxins in monocyte dysfunction, macrophage injury and the development and progression of atherosclerosis.

2. Protein-S-glutathionylation in macrophage recruitment and diabetic complications.

3. Role of betanectin in diabetic complications.

4. Monocytic Nox4: a novel NAD(P)H oxidase in monocyte differentiation, redox signaling and macrophage function.


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 accelerated atherosclerosis and renal injury in a new mouse model of diabetic complications.

Selected publications:

Complete Publication Listing