Photo of Joe GN Garcia
Joe GN Garcia
Professor, BIO5 Institute
Professor, Internal Medicine
Professor, Medicine
Professor, Pharmacology and Toxicology
Professor, Physiological Sciences - GIDP
Professor, Physiology
Primary Department
Medicine
Department Affiliations
Senior VP Health Sciences
Medicine
(520) 626-3151
skipgarcia@email.arizona.edu
Work Summary
The Garcia laboratory works to understand the molecular mechanisms of lung inflammatory processes, particularly those producing lung edema or vascular leak. The laboratory focus is to investigate gene discovery, protein function assessment, SNP discovery, genetic manipulation, in vivo testing, and candidate gene and biomarker identification, working to translate basic research into potential novel clinical therapies.
Research Interest
Dr. Garcia is an authority on the genetic basis of inflammatory lung disease (with an emphasis on health disparities) and on the mechanistic basis of lung vascular permeability. Using bench-to-bedside approaches, his lab has explored novel methods to prevent vascular leak and to restore endothelial cell barrier function and vascular integrity. This expertise in lung inflammation and vascular permeability provides a natural linkage to interrogation of lung vascular contribution to the development of lung metastases. Leveraging their genomic expertise, in recent years, Dr. Garcia's lab has identified vascular genes whose products are key participants in inflammatory lung injury that also play a role in cancer development. They have developed lung endothelial inflammatory gene expression profiles as well as diagnostic gene signatures influenced by MYLK and NAMPT that impact lung and breast cancer prognosis. This work with NAMPT led to development of a therapeutic NAMPT neutralizing antibody that has shown promise in treating lung cancer, melanoma, and chronic lymphocytic leukemia. Finally, Dr. Garcia's lab is also interested in the untoward effect of thoracic radiation and has been examining strategies designed to attenuate radiation–induced pneumonits, fibrosis and vascular leak. These collaborative and highly translational cancer research efforts have bolstered the overall mission of the University of Arizona Cancer Center.

Publications

Desai, A., Garcia, J. G., Yuan, J., Jacobson, J. J., Nair, V., Mitra, S., Tang, H., Gupta, G., & Gupta, A. (2017). Inhibition of the deubiquitinase, UCHL1, attenuates pulmonary hypertension.. American J Respiratory Critical Care Medicine.
Gross, C., Kellner, M., Wang, T., Lu, Q., Sun, X., Kangath, A., Zemskov, E., Kumar, S., Desai, A., Aggarwal, S., Golchov, B., Klinger, C., Verin, A. D., Catravas, J. D., Jacobsen, J. R., Yuan, J., Rafikov, R., Garcia, J. G., & Black, S. (2016). Lipopolysaccharide Induced Acute Lung Injury Involves the Nuclear Factor Kappa B Mediated Downregulation of the Transcription Factor SOX-18. Am J Respir Cell Mol Biol..
Champion, H. C., Champion, H. C., Vanderpool, R., Vanderpool, R., Garcia, J. G., Garcia, J. G., Yuan, J., Yuan, J., Abidov, A., Abidov, A., Desai, A., Desai, A., Knapp, S. M., Knapp, S. M., Knoper, S. R., Knoper, S. R., Hansen, L., Hansen, L., Simon, M., , Simon, M., et al. (2017). Treprostinil decreases right ventricular contractility but improves ejection fraction and exercise capacity in pulmonary arterial hypertension. European Respiratory J.
Singleton, P. A., Mambetsariev, N., Lennon, F. E., Mathew, B., Siegler, J. H., Moreno-Vinasco, L., Salgia, R., Moss, J., & Garcia, J. G. (2010). Methylnaltrexone potentiates the anti-angiogenic effects of mTOR inhibitors. Journal of angiogenesis research, 2(1), 5.

Recent cancer therapies include drugs that target both tumor growth and angiogenesis including mammalian target of rapamycin (mTOR) inhibitors. Since mTOR inhibitor therapy is associated with significant side effects, we examined potential agents that can reduce the therapeutic dose.

Sun, X., Mathew, B., Sammani, S., Jacobson, J. R., & Garcia, J. G. (2016). Simvastatin- Induced Sphingosine 1−Phosphate Receptor 1 Expression is KLF2-Dependent in Human Lung Endothelial Cells. Pulmonary Circulation.