Core B is a central resource for primary endothelial cell cultures and adenoviruses available for each of the four projects. This core facility will provide services for the following: 1) characterization and culture of primary human lung microvascular endothelial cells;2) isolation, characterization and culture of primary lung microvascular endothelial cells of mouse origin including those of different genetic mouse models and 3) amplification and purification of recombinant adenoviruses for the experiments proposed in the Projects as outiined in the Core description below. Human and mouse lung endothelial cell cultures are pivotal for the accomplishment of studies proposed in all four Projects. Specifically, Core B is critical for providing endothelial cells isolated from different genetic mouse models;e.g.,fiklGPF*'""""""""transgenic and Cav-1, eNOS, AKT-1, Src, Nox2 and PAR-1 knockout mice for Project 1;eNOS, iNOS, NADPH oxidase {p47phox and Nox2) and PAR-1 knockout mice for Project 2;Trpc6, TRPC1 and TRPC4, Src, PKC?, PAR-1 and EC-MLCK knockout mice for Project 3 and pi 10?, Src, Aktl, Cav-1, ICAM-1 mice for Project 4. In addition. Core B will provide amplification and purification of recombinant adenoviruses for all four Projects. The activities of this Core are essential for the success of the Program and successful completion of all aims in the four projects.

Agency
National Institute of Health (NIH)
Institute
National Heart, Lung, and Blood Institute (NHLBI)
Type
Research Program Projects (P01)
Project #
5P01HL060678-14
Application #
8620695
Study Section
Heart, Lung, and Blood Initial Review Group (HLBP)
Project Start
Project End
Budget Start
2014-03-01
Budget End
2015-02-28
Support Year
14
Fiscal Year
2014
Total Cost
$474,494
Indirect Cost
$172,268
Name
University of Illinois at Chicago
Department
Type
DUNS #
098987217
City
Chicago
State
IL
Country
United States
Zip Code
60612
Marsboom, Glenn; Rehman, Jalees (2018) Hypoxia Signaling in Vascular Homeostasis. Physiology (Bethesda) 33:328-337
Lv, Yang; Kim, Kyungho; Sheng, Yue et al. (2018) YAP Controls Endothelial Activation and Vascular Inflammation Through TRAF6. Circ Res 123:43-56
Christoforidis, Theodore; Driver, Tom G; Rehman, Jalees et al. (2018) Generation of controllable gaseous H2S concentrations using microfluidics. RSC Adv 8:4078-4083
Di, Anke; Xiong, Shiqin; Ye, Zhiming et al. (2018) The TWIK2 Potassium Efflux Channel in Macrophages Mediates NLRP3 Inflammasome-Induced Inflammation. Immunity 49:56-65.e4
Chen, Zhenlong; D S Oliveira, Suellen; Zimnicka, Adriana M et al. (2018) Reciprocal regulation of eNOS and caveolin-1 functions in endothelial cells. Mol Biol Cell 29:1190-1202
Le Master, Elizabeth; Huang, Ru-Ting; Zhang, Chongxu et al. (2018) Proatherogenic Flow Increases Endothelial Stiffness via Enhanced CD36-Mediated Uptake of Oxidized Low-Density Lipoproteins. Arterioscler Thromb Vasc Biol 38:64-75
Komarova, Yulia; Kruse, Kevin J; Mehta, Dolly et al. (2017) Response by Komarova et al to Letter Regarding Article, ""Protein Interactions at Endothelial Junctions and Signaling Mechanisms Regulating Endothelial Permeability"". Circ Res 120:e28
Mittal, Manish; Nepal, Saroj; Tsukasaki, Yoshikazu et al. (2017) Response by Mittal et al to Letter Regarding Article, ""Neutrophil Activation of Endothelial Cell-Expressed TRPM2 Mediates Transendothelial Neutrophil Migration and Vascular Injury"". Circ Res 121:e87
Soni, Dheeraj; Regmi, Sushil C; Wang, Dong-Mei et al. (2017) Pyk2 phosphorylation of VE-PTP downstream of STIM1-induced Ca2+ entry regulates disassembly of adherens junctions. Am J Physiol Lung Cell Mol Physiol 312:L1003-L1017
Oliveira, Suellen D S; Castellon, Maricela; Chen, Jiwang et al. (2017) Inflammation-induced caveolin-1 and BMPRII depletion promotes endothelial dysfunction and TGF-?-driven pulmonary vascular remodeling. Am J Physiol Lung Cell Mol Physiol 312:L760-L771

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