Rationale and Aims: This application proposes to establish a research-based training program for physician-scientists and Ph.D. scientists in Nephrology and Hypertension at the Oregon Health and Science University.
The aim i s to prepare individuals for successful academic/scientific careers, by providing intensive training in clinical or laboratory-based, hypothesis-driven, basic and disease- oriented research in an interactive environment. The premise of this program is that the need for skilled physician-investigators will increase over time as developments in molecular-based medicine have greater impact on the prevention, diagnosis, and treatment of hypertension and renal disease. Structure of the Training Program: This application seeks support for 3 postdoctoral trainees (2 in the first year). For M.D. scientists, research training will be preceded by a year of clinical training, with formal educational activities which teach the scientific basis of nephrology. The clinical year will be funded through institutional resources. During this year, candidates will be matched with appropriate mentors in preparation for the research period. Subsequent years (2 or more) will be devoted to laboratory or clinical research, funded by this grant. For Ph.D. scientists, the research training will be preceded by successful completion of a Ph.D. program in a basic science discipline. For all candidates, research activities will be supplemented by journal clubs, laboratory group meetings, and course work tailored to the trainee's individual scientific goals. Research Areas and Disciplines: This program will bring together investigators from the Divisions of Nephrology and Cardiology, Dept. of Medicine;the Division of Pediatric Nephrology, Dept. of Pediatrics;the Departments of Medical Informatics and Clinical Epidemiology, Biochemistry, and Physiology and Pharmacology;and other associated faculty. Investigators and trainees will be grouped into interrelated basic thematic interest areas: Hypertension, Chronic Kidney Disease, and Renal Physiology/Signaling. Within each group will be represented scientists with expertise in molecular biology, physiology, vascular biology, and related disciplines as appropriate. State-of-the-art laboratories at the Oregon Health and Science University and the Portland VA Medical Center will serve as training facilities for bench research. The clinical research projects have access to the OHSU GCRC, and the Human Investigations, and Masters in Clinical Research or Public Health programs. Relevance: This program will train investigators in the study of hypertension and chronic kidney disease, which are both major and growing public health problems in the U.S.
| Cornelius, Ryan J; Si, Jinge; Cuevas, Catherina A et al. (2018) Renal COP9 Signalosome Deficiency Alters CUL3-KLHL3-WNK Signaling Pathway. J Am Soc Nephrol 29:2627-2640 |
| Lazelle, Rebecca A; McCully, Belinda H; Terker, Andrew S et al. (2016) Renal Deletion of 12 kDa FK506-Binding Protein Attenuates Tacrolimus-Induced Hypertension. J Am Soc Nephrol 27:1456-64 |
| Terker, Andrew S; Yarbrough, Bethzaida; Ferdaus, Mohammed Z et al. (2016) Direct and Indirect Mineralocorticoid Effects Determine Distal Salt Transport. J Am Soc Nephrol 27:2436-45 |
| Zhang, Chong; Meermeier, Nicholas P; Terker, Andrew S et al. (2016) Degradation by Cullin 3 and effect on WNK kinases suggest a role of KLHL2 in the pathogenesis of Familial Hyperkalemic Hypertension. Biochem Biophys Res Commun 469:44-48 |
| Terker, Andrew S; Zhang, Chong; Erspamer, Kayla J et al. (2016) Unique chloride-sensing properties of WNK4 permit the distal nephron to modulate potassium homeostasis. Kidney Int 89:127-34 |
| Ellison, David H; Terker, Andrew S; Gamba, Gerardo (2016) Potassium and Its Discontents: New Insight, New Treatments. J Am Soc Nephrol 27:981-9 |
| Terker, Andrew S; Ellison, David H (2015) Renal mineralocorticoid receptor and electrolyte homeostasis. Am J Physiol Regul Integr Comp Physiol 309:R1068-70 |
| Terker, Andrew S; Zhang, Chong; McCormick, James A et al. (2015) Potassium modulates electrolyte balance and blood pressure through effects on distal cell voltage and chloride. Cell Metab 21:39-50 |
| McCormick, James A; Yang, Chao-Ling; Zhang, Chong et al. (2014) Hyperkalemic hypertension-associated cullin 3 promotes WNK signaling by degrading KLHL3. J Clin Invest 124:4723-36 |
| Liu, Ya Ni; Khangura, Jaspreet; Xie, Aris et al. (2013) Renal retention of lipid microbubbles: a potential mechanism for flank discomfort during ultrasound contrast administration. J Am Soc Echocardiogr 26:1474-81 |
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