Report From the May 1996 National Advisory Council Meeting of NHLBI (National Heart, Lung, Blood Institute)

1996 ◽  
Author(s):  
Karen A. Matthews ◽  
Keyword(s):  
Advisory Council ◽  
Council Meeting ◽  
Blood Institute ◽  
National Heart ◽  
National Heart Lung ◽  
National Advisory Council

scholarly journals Funding mechanisms and program management at the National Heart, Lung, and Blood Institute: confronting new challenges and exploring new opportunities

Blood ◽  
2011 ◽  
Vol 118 (20) ◽  
pp. 5380-5382 ◽  
Author(s):  
Susan B. Shurin
Keyword(s):  
Early Stage ◽  
Advisory Council ◽  
Fiscal Year ◽  
Blood Institute ◽  
Resource Limitations ◽  
National Heart ◽  
National Heart Lung ◽  
Funding Mechanisms ◽  
Long Term Impact ◽  
First Time

Abstract Over the past 8 years, the National Institutes of Health (NIH) budget appropriation has lost purchasing power, with erosion of the benefits of the doubling of the budget less than a decade ago. For the first time in 40 years, the NIH appropriation in fiscal year 2011 was 1% less than in the previous year. The National Heart, Lung, and Blood Institute (NHLBI) has been closely managing its funds to protect its core functions: support and conduct of research, and training of biomedical research scientists. Rigorous evaluations of funding mechanisms, management of clinical studies, set-aside programs and funding guidelines are designed to help the Institute, in consultation with its advisory council, to minimize the long-term impact of extreme resource limitations on the advance and conduct of science. This report describes some recent actions taken by the NHLBI to maximize support for investigator-initiated research, maintain a balanced portfolio, and provide as much support as possible for established and early-stage investigators.

scholarly journals 4369 Reprogramming of vascular smooth muscle cells to multipotent progenitor cells contributes to progression of atherosclerosis

2020 ◽  
Vol 4 (s1) ◽  
pp. 102-102
Author(s):  
Allison Milfred Dubner ◽  
Sizhao Lu ◽  
Austin Jolly ◽  
Keith Strand ◽  
Marie Mutryn ◽  
...  
Keyword(s):  
Flow Cytometry ◽  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Progenitor Cells ◽  
Coronary Arteries ◽  
Lineage Tracing ◽  
Plaque Progression ◽  
Blood Institute ◽  
National Heart ◽  
National Heart Lung

OBJECTIVES/GOALS: Our lab previously identified a population of vascular smooth muscle (SMC)-derived progenitor cells (AdvSca1-SM) which expand robustly in response to disease and can differentiate into multiple cell types. We now aim to define the role of these AdvSca1-SM cells in atherosclerotic plaque progression. METHODS/STUDY POPULATION: Goal one uses SMC lineage tracing mice and a model of atherosclerosis to track reprogramming of SMCs to AdvSca1-SM cells in the setting of disease. Arteries are analyzed using flow cytometry and immunofluorescence to quantify changes in number of mature SMCs and AdvSca1-SM cells. Goal two uses AdvSca1-SM lineage tracing mice with high cholesterol-induced atherosclerosis and plaque neovascularization. Arteries are analyzed to quantify expansion of AdvSca1-SM cells, subsequent re-differentiation into mature SMC, endothelial cells, or macrophages, and contribution to plaque neovascularization. Mechanistic findings from both goals are being investigated in diseased human coronary arteries. RESULTS/ANTICIPATED RESULTS: Flow cytometry from SMC lineage tracing mice revealed a 7- to 13-fold expansion of AdvSca1-SM cells in carotid arteries (p<0.001) and aortas (p = 0.03) after 6 weeks of western diet; no differences in macrophage numbers were observed. Additional SMC and AdvSca1-SM cell lineage tracing mice are on atherogenic diets to assess early and advanced atherosclerosis. We predict that AdvSca1-SM cells will contribute to macrophage accumulation as well as plaque neovascularization in the setting of severe atherosclerosis. Translational relevance of mechanisms driving SMC reprogramming and AdvSca1-SM cell contribution to plaque progression are being applied to studies of diseased human coronary arteries. DISCUSSION/SIGNIFICANCE OF IMPACT: Our data suggest a role for AdvSca1-SM cells in atherosclerosis. Ongoing work will clarify the mechanisms driving plaque-associated AdvSca1-SM expansion and define the ultimate fates of these cells. In vivo modulation of this process could provide the basis for future anti-atherosclerotic therapies. CONFLICT OF INTEREST DESCRIPTION: AD - CCTSI TOTTS TL1TR002533; SL - 18POST34030397 from the American Heart Association; AJ – no conflicts; KS - 1F31HL147393 from the National Heart, Lung, and Blood Institute, NIH; MM – no conflicts; RT – no conflicts; KSM – no conflicts; RAN - R01CA236222 from the National Cancer Institute, NIH, and 2018-03 from the Lungevity Foundation; and MCMW-E - R01 HL121877 from the National Heart, Lung, and Blood Institute, NIH, and 25A8679 from the Chernowitz Foundation.

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