For the individual projects, gene expression analyses will be provided for specific cellular, animal, and clinical phenotypes. Importantly, this core lab will develop custom targeted gene expression and miRNA arrays that will provide the capacity to examine and directly compare related gene sets involved in endothelial function, mitochondrial biogenesis and function, reactive oxygen species, adipocytes, macrophages and hypoxia/angiogenesis. The Gene Expression Core has previously collaborated or published with Drs. Gokce and Vita and has begun studying miRNA and high-throughput gene expression with Drs. Cohen and Walsh. The Gene Expression Core Laboratory is an established facility with automated robotic pipeting using computerized programs, automated RNA isolation, storage, and custom chip capacity. The Laboratory is already involved in high-throughput analysis of over 10,000 subjects'gene expression, miRNA, and protein samples from various clinical projects. The laboratory has also assisted investigators in gene expression analysis from small volume tissue using murine and cell culture models. Importantly, there will be developed an established panel of genes and miRNA that will be compared across studies to determine the mechanistic overlap between specific inflammatory states and metabolic diseases and the role individual cell types play in endothelial and vascular disease (see Table 1).

Agency
National Institute of Health (NIH)
Institute
National Heart, Lung, and Blood Institute (NHLBI)
Type
Research Program Projects (P01)
Project #
5P01HL081587-08
Application #
8438335
Study Section
Heart, Lung, and Blood Initial Review Group (HLBP)
Project Start
Project End
Budget Start
2013-03-01
Budget End
2014-02-28
Support Year
8
Fiscal Year
2013
Total Cost
$209,525
Indirect Cost
$81,531
Name
Boston University
Department
Type
DUNS #
604483045
City
Boston
State
MA
Country
United States
Zip Code
02118
Maruyama, Sonomi; Nakamura, Kazuto; Papanicolaou, Kyriakos N et al. (2016) Follistatin-like 1 promotes cardiac fibroblast activation and protects the heart from rupture. EMBO Mol Med 8:949-66
Nakamura, Kazuto; Sano, Soichi; Fuster, José J et al. (2016) Secreted Frizzled-related Protein 5 Diminishes Cardiac Inflammation and Protects the Heart from Ischemia/Reperfusion Injury. J Biol Chem 291:2566-75
Fetterman, Jessica L; Holbrook, Monica; Flint, Nir et al. (2016) Restoration of autophagy in endothelial cells from patients with diabetes mellitus improves nitric oxide signaling. Atherosclerosis 247:207-17
Krzywanski, David M; Moellering, Douglas R; Westbrook, David G et al. (2016) Endothelial Cell Bioenergetics and Mitochondrial DNA Damage Differ in Humans Having African or West Eurasian Maternal Ancestry. Circ Cardiovasc Genet 9:26-36
Tampakakis, Emmanouil; Tabit, Corey E; Holbrook, Monika et al. (2016) Intravenous Lipid Infusion Induces Endoplasmic Reticulum Stress in Endothelial Cells and Blood Mononuclear Cells of Healthy Adults. J Am Heart Assoc 5:
Fetterman, Jessica L; Holbrook, Monica; Westbrook, David G et al. (2016) Mitochondrial DNA damage and vascular function in patients with diabetes mellitus and atherosclerotic cardiovascular disease. Cardiovasc Diabetol 15:53
Bretón-Romero, Rosa; Feng, Bihua; Holbrook, Monika et al. (2016) Endothelial Dysfunction in Human Diabetes Is Mediated by Wnt5a-JNK Signaling. Arterioscler Thromb Vasc Biol 36:561-9
Lee, Richard T; Walsh, Kenneth (2016) The Future of Cardiovascular Regenerative Medicine. Circulation 133:2618-25
Fuster, José J; Ouchi, Noriyuki; Gokce, Noyan et al. (2016) Obesity-Induced Changes in Adipose Tissue Microenvironment and Their Impact on Cardiovascular Disease. Circ Res 118:1786-807
Mohandas, Appesh; Suboc, Tisha B; Wang, Jingli et al. (2015) Mineralocorticoid exposure and receptor activity modulate microvascular endothelial function in African Americans with and without hypertension. Vasc Med 20:401-8

Showing the most recent 10 out of 165 publications