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
Di, Anke; Mehta, Dolly; Malik, Asrar B (2016) ROS-activated calcium signaling mechanisms regulating endothelial barrier function. Cell Calcium 60:163-71
Tauseef, Mohammad; Farazuddin, Mohammad; Sukriti, Sukriti et al. (2016) Transient receptor potential channel 1 maintains adherens junction plasticity by suppressing sphingosine kinase 1 expression to induce endothelial hyperpermeability. FASEB J 30:102-10
Gong, Haixia; An, Shejuan; Sassmann, Antonia et al. (2016) PAR1 Scaffolds TGFβRII to Downregulate TGF-β Signaling and Activate ESC Differentiation to Endothelial Cells. Stem Cell Reports 7:1050-1058
Rajput, Charu; Tauseef, Mohammad; Farazuddin, Mohammad et al. (2016) MicroRNA-150 Suppression of Angiopoetin-2 Generation and Signaling Is Crucial for Resolving Vascular Injury. Arterioscler Thromb Vasc Biol 36:380-8
Ebenezer, David L; Fu, Panfeng; Suryadevara, Vidyani et al. (2016) Epigenetic regulation of pro-inflammatory cytokine secretion by sphingosine 1-phosphate (S1P) in acute lung injury: Role of S1P lyase. Adv Biol Regul :
Zimnicka, Adriana M; Husain, Yawer S; Shajahan, Ayesha N et al. (2016) Src-dependent phosphorylation of caveolin-1 Tyr-14 promotes swelling and release of caveolae. Mol Biol Cell 27:2090-106
Jiang, Ying; Sverdlov, Maria S; Toth, Peter T et al. (2016) Phosphatidic Acid Produced by RalA-activated PLD2 Stimulates Caveolae-mediated Endocytosis and Trafficking in Endothelial Cells. J Biol Chem 291:20729-38
Liu, Yuru; Kumar, Varsha Suresh; Zhang, Wei et al. (2015) Activation of type II cells into regenerative stem cell antigen-1(+) cells during alveolar repair. Am J Respir Cell Mol Biol 53:113-24
Geyer, Melissa; Huang, Fei; Sun, Ying et al. (2015) Microtubule-Associated Protein EB3 Regulates IP3 Receptor Clustering and Ca(2+) Signaling in Endothelial Cells. Cell Rep 12:79-89
Zhang, Xianming; Brovkovych, Viktor; Zhang, Yongkang et al. (2015) Downregulation of kinin B1 receptor function by B2 receptor heterodimerization and signaling. Cell Signal 27:90-103

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