Research in the field of vascular biology has changed how we prevent, monitor, and treat cardiovascular disease. In particular, efforts in the last fifty years provided transformative advancements in patient care, raised life expectancy, and improved the quality of life of those individuals affected by vascular pathologies. However, challenges still remain. Furthermore, the improvements in reparative surgery and treatment of previously lethal cardiovascular anomalies, brought to light new pathologies associated with a population that now survives congenital diseases. It is through training of the next generation that we will be able to make constant improvements in cardiovascular care to address emerging clinical problems. This proposal seeks renewal for the Vascular Biology Training Program (VBTP) at UCLA. Entering its 4th cycle, the program has provided training for 46 graduate students and post-doctoral fellows since 2002. Its degree of success can be assessed by the high percentage of trainees now in academic and industry positions and by the caliber of the 169 studies published by our trainees. In this next iteration of the program, our central goal remains to offer robust, interdisciplinary training to the next generation of vascular biologists. To achieve this goal, we are renewing the structure of our educational approach to respond to the more diverse needs of our trainees and the expanding demands of the future workforce. Specifically, the program has evolved to adopt a multi-mentorship approach, incorporate training in emerging technologies, and create opportunities for interactive exposure to industry and medicine. In this manner, we aim to develop scientists who are intellectually broad and have technical versatility, able to integrate information from multiple fields, and apply this information toward the resolution of emerging challenges in the field. The program also places a strong emphasis in career development, research integrity, and on enlarging the pool of underrepresented scientists. As the only Vascular Biology Training Grant in the Los Angeles area and one of eight in the state of California, our program is sought-after by a large pool of candidates. This allows us to select highly qualified and committed trainees and to build a community of scholars with strong focus in vascular biology. Importantly, UCLA has a large number of interdisciplinary groups interested in diverse aspects of vascular biology and located next to a large research hospital. It is this community that constitues the pillars of a unique training program for the next generation of scientists. Here, we request funds to continue the support for 7 pre- and 3 post-doctoral fellows/year, in which 2-3 new graduate students and 1-2 post-doctoral fellows will enter the program each year. The previous success of the program and the commitment of its faculty has engendered enthusiasm within the School of Medicine, College, and the Graduate Division at UCLA. Each of these entities have pledged institutional support and programatic synergy to accomplish the renewed goals of this program.

Public Health Relevance

The Vascular Biology Training Program at UCLA strives to offer scientific training and professional enhancement for the next generation of scientists who reflect our diversity and ethical standards and who are poised to take advantage of interdisciplinary activities in basic research as well as in novel strategies for the prevention and treatment of cardiovascular disease. The major foundation of the program is the training provided by our faculty, the wealth of interactions with clinical and basic scientists, and our tailored approach to professional development.

Agency
National Institute of Health (NIH)
Institute
National Heart, Lung, and Blood Institute (NHLBI)
Type
Institutional National Research Service Award (T32)
Project #
2T32HL069766-16A1
Application #
9417494
Study Section
NHLBI Institutional Training Mechanism Review Committee (NITM)
Program Officer
Wang, Wayne C
Project Start
2002-04-01
Project End
2023-03-31
Budget Start
2018-04-01
Budget End
2019-03-31
Support Year
16
Fiscal Year
2018
Total Cost
Indirect Cost
Name
University of California Los Angeles
Department
Biochemistry
Type
Schools of Arts and Sciences
DUNS #
092530369
City
Los Angeles
State
CA
Country
United States
Zip Code
90095
Park, Shuin; Ranjbarvaziri, Sara; Lay, Fides D et al. (2018) Genetic Regulation of Fibroblast Activation and Proliferation in Cardiac Fibrosis. Circulation 138:1224-1235
Ziyad, Safiyyah; Riordan, Jesse D; Cavanaugh, Ann M et al. (2018) A Forward Genetic Screen Targeting the Endothelium Reveals a Regulatory Role for the Lipid Kinase Pi4ka in Myelo- and Erythropoiesis. Cell Rep 22:1211-1224
Salehi, Sahar; Sosa, Rebecca A; Jin, Yi-Ping et al. (2018) Outside-in HLA class I signaling regulates ICAM-1 clustering and endothelial cell-monocyte interactions via mTOR in transplant antibody-mediated rejection. Am J Transplant 18:1096-1109
Chella Krishnan, Karthickeyan; Kurt, Zeyneb; Barrere-Cain, Rio et al. (2018) Integration of Multi-omics Data from Mouse Diversity Panel Highlights Mitochondrial Dysfunction in Non-alcoholic Fatty Liver Disease. Cell Syst 6:103-115.e7
Erbilgin, Ayca; Seldin, Marcus M; Wu, Xiuju et al. (2018) Transcription Factor Zhx2 Deficiency Reduces Atherosclerosis and Promotes Macrophage Apoptosis in Mice. Arterioscler Thromb Vasc Biol 38:2016-2027
Seldin, Marcus M; Koplev, Simon; Rajbhandari, Prashant et al. (2018) A Strategy for Discovery of Endocrine Interactions with Application to Whole-Body Metabolism. Cell Metab 27:1138-1155.e6
Mack, Julia J; Mosqueiro, Thiago S; Archer, Brian J et al. (2017) NOTCH1 is a mechanosensor in adult arteries. Nat Commun 8:1620
Rau, Christoph D; Vondriska, Thomas M (2017) DNA Methylation and Human Heart Failure: Mechanisms or Prognostics. Circulation 136:1545-1547
Hu, Xuchen; Dallinga-Thie, Geesje M; Hovingh, G Kees et al. (2017) GPIHBP1 autoantibodies in a patient with unexplained chylomicronemia. J Clin Lipidol 11:964-971
Allan, Christopher M; Jung, Cris J; Larsson, Mikael et al. (2017) Mutating a conserved cysteine in GPIHBP1 reduces amounts of GPIHBP1 in capillaries and abolishes LPL binding. J Lipid Res 58:1453-1461

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