Core C Administrative The purpose of this Program is to bring together a team of investigators to focus on the pathobiology of two important disease states, chronic allergic asthma and idiopathic pulmonary fibrosis using both state-of-the-art animal modeling and human samples. The goals of this Program are to improve our understanding of the mechanisms that contribute to disease progression and identify novel therapeutic targets to combat lung fibrosis whether it occurs in the airway or in the interstifium of the lung. The Program brings together a team of scienfists and physician scientists with complementary skills to work as a unit on these important problems. In order to coordinate these efforts we propose an Administrative Core to facilitate interactions and adherence to NIH regulations regarding management of P01 proposals. We propose the following Specific Aims: Coordinate and facilitate administration of the Program between Project Leaders and Core Leaders. Coordinate and facilitate administration of the Program between investigators, internal and external advisors and an enrichment program organized to maximize scientific productivity.

Public Health Relevance

There are no effective therapeutic approaches to limit airway remodeling and interstitial fibrosis. Our proposal brings together experts in surfactant biology, interstitial fibrosis and translational asthma research and will provide mechanistic insights into how endogenous host factors regulate chronic inflammation, airway remodeling and interstitial fibrosis in mouse and man with the potential to provide new therapies for these severe diseases.

Agency
National Institute of Health (NIH)
Institute
National Heart, Lung, and Blood Institute (NHLBI)
Type
Research Program Projects (P01)
Project #
5P01HL108793-03
Application #
8680339
Study Section
Special Emphasis Panel (ZHL1-CSR-S)
Project Start
Project End
Budget Start
2014-06-01
Budget End
2015-05-31
Support Year
3
Fiscal Year
2014
Total Cost
$240,878
Indirect Cost
$65,775
Name
Cedars-Sinai Medical Center
Department
Type
DUNS #
075307785
City
Los Angeles
State
CA
Country
United States
Zip Code
90048
Xie, Ting; Wang, Yizhou; Deng, Nan et al. (2018) Single-Cell Deconvolution of Fibroblast Heterogeneity in Mouse Pulmonary Fibrosis. Cell Rep 22:3625-3640
Liang, Jiurong; Liu, Ningshan; Liu, Xue et al. (2018) MK2 Inhibition Attenuates Fibroblast Invasion and Severe Lung Fibrosis. Am J Respir Cell Mol Biol :
Xie, Ting; Liang, Jiurong; Geng, Yan et al. (2017) MicroRNA-29c Prevents Pulmonary Fibrosis by Regulating Epithelial Cell Renewal and Apoptosis. Am J Respir Cell Mol Biol 57:721-732
Liang, Jiurong; Zhang, Yanli; Xie, Ting et al. (2016) Hyaluronan and TLR4 promote surfactant-protein-C-positive alveolar progenitor cell renewal and prevent severe pulmonary fibrosis in mice. Nat Med 22:1285-1293
Yu, Yen-Rei A; Hotten, Danielle F; Malakhau, Yuryi et al. (2016) Flow Cytometric Analysis of Myeloid Cells in Human Blood, Bronchoalveolar Lavage, and Lung Tissues. Am J Respir Cell Mol Biol 54:13-24
Li, Yuejuan; Liang, Jiurong; Yang, Ting et al. (2016) Hyaluronan synthase 2 regulates fibroblast senescence in pulmonary fibrosis. Matrix Biol 55:35-48
Xu, Yan; Mizuno, Takako; Sridharan, Anusha et al. (2016) Single-cell RNA sequencing identifies diverse roles of epithelial cells in idiopathic pulmonary fibrosis. JCI Insight 1:e90558
Liang, Jiurong; Jiang, Dianhua; Noble, Paul W (2016) Hyaluronan as a therapeutic target in human diseases. Adv Drug Deliv Rev 97:186-203
Xie, Ting; Liang, Jiurong; Liu, Ningshan et al. (2016) Transcription factor TBX4 regulates myofibroblast accumulation and lung fibrosis. J Clin Invest 126:3063-79
Dong, Yingying; Geng, Yan; Li, Lian et al. (2015) Blocking follistatin-like 1 attenuates bleomycin-induced pulmonary fibrosis in mice. J Exp Med 212:235-52

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