Austin M. Guo, Ph.D., has more than 20 years of experience in the areas of 20-HETE, cancer, and angiogenesis and has published 17 original research papers on these subjects. Dr. Guo has extensive training in cell culturing, in vitro and in vivo models to study angiogenesis, immune-fluorescent microscopy, immunoassay, and various molecular techniques. Over the past 13 years, he has gained additional experience working with stem cells, small animal models, and has acquired experience in flow cytometry. Dr. Guo has fostered collaborations both internally and externally with several world-renowned scientists in the field of eicosanoid research, stem cell biology, and vascular biology. Aside from his continued passion for translational research, Dr. Guo is currently a full-time educator who is extensively involved in course teaching across the medical, dental, and graduate schools. His major administrative function involves directing the Women in Scientific Entrepreneurship-Summer Trainee in Academic Research (WISE-STAR) program and the Master’s Degree Program in Interdisciplinary Biomedical Sciences (iBMS).
Education
- Ph.D., Cancer Biology, Wayne State University
- B.S., Biotechnology, St. Cloud State University
Areas of Expertise
- Cancer Biology
- Angiogenesis
- Eicosanoids
Honors and Awards
- POLM/Elsevier Young Investigator Award
- NIEHS travel awards
Research
Dr. Guo's research interests are centered on the area of vascular pathophysiology, particularly the study of the mechanisms of a bioactive lipid known as 20-hydroxyeicosatetraenoic acid (20-HETE)'s effect on pathological angiogenesis. Currently, his lab is specifically focused on understanding the role of Cytochrome P450 4A-derived eicosanoids 20-HETE, in the regulation of ischemia-induced angiogenesis. Dr. Guo's lab has demonstrated that the CYP4A/20-HETE axis regulates ischemic angiogenesis via its collective actions on EC, EPC as well as inflammatory neutrophils. They found that 20-HETE level is markedly upregulated in ischemic tissue. Inhibition of 20-HETE synthesis or antagonizing 20-HETE actions decreases ischemia-induced compensatory neovascularization in vivo. Recent works from the group further identified that inflammatory neutrophils and their associated Myeloperoxidase and Hypochlorous acid significantly contribute to the increase 20-HETE production in ischemic tissue, potentially a novel therapeutic target. Stemming from their studies in the role of the CYP4A-20-HETE axis in regulation of angiogenic processes, they are also interested in the regulation of cancer growth by the CYP4A/F-20-HETE system, potentially via a tumor-mediated angiogenesis-dependent mechanism. Pharmacological inhibitors of 20-HETE synthases and 20-HETE antagonists have been shown to decrease the growth of some cancers both in vitro and in vivo, suggesting the CYP4A-20-HETE axis may also be a novel target for treating some cancers.
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Publications
Teaching Responsibilities
- M1/M2 SOM Integrated Curriculum
- Dental Pharmacology
- Graduate Pharmacology
