Function of Core 'A'as a resource of the program project grant: The Lesion Analysis/ Biostatistics Core will work with each of the three projects to facilitate quantitative and qualitative assessment of lesions with special emphasis on markers of lesion progression. Specific services will include A) quantification of lesions of both the proximal aorta and brachio-cephalic artery (BCA) using cross-sectional analysis, B) quantification of lesions using en face aortic preparations, C) determination of the cellular composition of lesions, D) quantification of markers of lesion progression including necrotic core and fibrous cap formation as well as intra-plaque matrix deposition, E) staining for markers of apoptosis, F) detection of ER stress and UPR activation and G) quantification of gene expression using laser-capture microdissection (LCM). In addition, the Core will provide Biostatistical support, through the expertise and services of Dr Rajasekhar Ramakrishnan. This will be important in the design of the mouse studies and in the analysis of atherosclerosis quantitative data and gene expression array analysis. Or. Ramakrishnan has particular expertise in these areas and has worked extensively with Drs. Tabas and Tall on previous projects.

Agency
National Institute of Health (NIH)
Institute
National Heart, Lung, and Blood Institute (NHLBI)
Type
Research Program Projects (P01)
Project #
5P01HL087123-03
Application #
7883471
Study Section
Heart, Lung, and Blood Initial Review Group (HLBP)
Project Start
Project End
Budget Start
2009-07-01
Budget End
2010-06-30
Support Year
3
Fiscal Year
2009
Total Cost
$164,483
Indirect Cost
Name
Columbia University (N.Y.)
Department
Type
DUNS #
621889815
City
New York
State
NY
Country
United States
Zip Code
10032
Molusky, Matthew M; Hsieh, Joanne; Lee, Samuel X et al. (2018) Metformin and AMP Kinase Activation Increase Expression of the Sterol Transporters ABCG5/8 (ATP-Binding Cassette Transporter G5/G8) With Potential Antiatherogenic Consequences. Arterioscler Thromb Vasc Biol 38:1493-1503
Cai, Bishuang; Kasikara, Canan; Doran, Amanda C et al. (2018) MerTK signaling in macrophages promotes the synthesis of inflammation resolution mediators by suppressing CaMKII activity. Sci Signal 11:
Accili, Domenico (2018) Insulin Action Research and the Future of Diabetes Treatment: The 2017 Banting Medal for Scientific Achievement Lecture. Diabetes 67:1701-1709
Haeusler, Rebecca A; McGraw, Timothy E; Accili, Domenico (2018) Biochemical and cellular properties of insulin receptor signalling. Nat Rev Mol Cell Biol 19:31-44
Kraakman, Michael J; Liu, Qiongming; Postigo-Fernandez, Jorge et al. (2018) PPAR? deacetylation dissociates thiazolidinedione's metabolic benefits from its adverse effects. J Clin Invest 128:2600-2612
Ghorpade, Devram S; Ozcan, Lale; Zheng, Ze et al. (2018) Hepatocyte-secreted DPP4 in obesity promotes adipose inflammation and insulin resistance. Nature 555:673-677
Fredman, Gabrielle; Tabas, Ira (2017) Boosting Inflammation Resolution in Atherosclerosis: The Next Frontier for Therapy. Am J Pathol 187:1211-1221
Doran, Amanda C; Ozcan, Lale; Cai, Bishuang et al. (2017) CAMKII? suppresses an efferocytosis pathway in macrophages and promotes atherosclerotic plaque necrosis. J Clin Invest 127:4075-4089
Tabas, Ira; Lichtman, Andrew H (2017) Monocyte-Macrophages and T Cells in Atherosclerosis. Immunity 47:621-634
Cai, Bishuang; Thorp, Edward B; Doran, Amanda C et al. (2017) MerTK receptor cleavage promotes plaque necrosis and defective resolution in atherosclerosis. J Clin Invest 127:564-568

Showing the most recent 10 out of 98 publications