The overall goals of Core C are to provide (i) fluorescence, confocal, and electron microscopy support and (ii) physiological support for lung perfusion experiments proposed in all projects. Centralization of the imaging and physiological support within a single core reflects the emphasis that P.l.s have placed on imaging and physiological studies in lung models. Core 0 is essential in order to fulfill the objectives of all projeds. In addition to the research support. Core 0 personnel will also provide training for project participants in these methodologies. Core 0 will provide expertise, resources, and equipment for performing lung studies in the knockout mouse models and other mouse models in which proteins of interest are expressed through gene delivery via liposomes. Core 0 will provide expertise forthe transfection of cDNAs in mouse lung microvessels using cationic liposomes. The physiological support component will provide standardized methods for quantification of lung vascular permeability in normal and genetically modified mice. This will include measurement of pulmonary capillary filtration coefficient and vessel wall albumin permeability surface-area product. The methods to be used have been developed specifically for the mouse lung. In addition, lung vascular albumin permeability and the routes of albumin transport will be assessed by electron microscopy and morphometric analysis using described methods. In the imaging component. Core C will provide resources and expertise for (i) live cell and fixed specimen fluorescence, confocal, and TIRF (total internal reflective fluorescence) microscopy and (ii) electron microscopy. Also Core C will provide assessment of expression of fluorescent or tagged proteins by fluorescence and confocal microscopy as described.

Agency
National Institute of Health (NIH)
Institute
National Heart, Lung, and Blood Institute (NHLBI)
Type
Research Program Projects (P01)
Project #
5P01HL077806-09
Application #
8521349
Study Section
Heart, Lung, and Blood Initial Review Group (HLBP)
Project Start
Project End
Budget Start
2013-08-01
Budget End
2014-07-31
Support Year
9
Fiscal Year
2013
Total Cost
$192,360
Indirect Cost
$69,837
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
Tran, Khiem A; Zhang, Xianming; Predescu, Dan et al. (2016) Endothelial β-Catenin Signaling Is Required for Maintaining Adult Blood-Brain Barrier Integrity and Central Nervous System Homeostasis. Circulation 133:177-86
Yan, Zhibo; Wang, Zhen-Guo; Segev, Nava et al. (2016) Rab11a Mediates Vascular Endothelial-Cadherin Recycling and Controls Endothelial Barrier Function. Arterioscler Thromb Vasc Biol 36:339-49
Huang, Xiaojia; Dai, Zhiyu; Cai, Lei et al. (2016) Endothelial p110γPI3K Mediates Endothelial Regeneration and Vascular Repair After Inflammatory Vascular Injury. Circulation 133:1093-103
Mittal, Manish; Tiruppathi, Chinnaswamy; Nepal, Saroj et al. (2016) TNFα-stimulated gene-6 (TSG6) activates macrophage phenotype transition to prevent inflammatory lung injury. Proc Natl Acad Sci U S A 113:E8151-E8158
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
Dai, Zhiyu; Li, Ming; Wharton, John et al. (2016) Prolyl-4 Hydroxylase 2 (PHD2) Deficiency in Endothelial Cells and Hematopoietic Cells Induces Obliterative Vascular Remodeling and Severe Pulmonary Arterial Hypertension in Mice and Humans Through Hypoxia-Inducible Factor-2α. Circulation 133:2447-58
Weber, Evan W; Han, Fei; Tauseef, Mohammad et al. (2015) TRPC6 is the endothelial calcium channel that regulates leukocyte transendothelial migration during the inflammatory response. J Exp Med 212:1883-99
Baig, Mirza Saqib; Zaichick, Sofia V; Mao, Mao et al. (2015) NOS1-derived nitric oxide promotes NF-κB transcriptional activity through inhibition of suppressor of cytokine signaling-1. J Exp Med 212:1725-38

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