Summary of study ST000143

This data is available at the NIH Common Fund's National Metabolomics Data Repository (NMDR) website, the Metabolomics Workbench, https://www.metabolomicsworkbench.org, where it has been assigned Project ID PR000219. The data can be accessed directly via it's Project DOI: 10.21228/M8359Z This work is supported by NIH grant, U2C- DK119886.

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Study IDST000143
Study TitleMetabolic analysis of Normal Mouse Lung Fiboblasts with/without TGFbeta treatment (Part 1)
Study TypeGlycolysis/TCA/Nucleotide analysis (tissue/cells)
Study SummaryThis study is a part of series performed for the same researcher through pilot/feasibility grant program, so the publication is relevant reference for other studies, see the project for this study. This specific experiment is a small pilot study to establish method performance, it includes four biological replicas of identical cell cultures after the identical treatment and a single tissue sample.
Institute
University of Michigan
DepartmentBiomedical Research Core Facilities
LaboratoryMetabolomics core
Last NameKachman
First NameMaureen
Address6300 Brehm Tower, 1000 Wall Street, Ann Arbor, MI 48105-5714
Email mkachman@umich.edu
Submit Date2015-03-13
Num Groups4
Total Subjects21
Raw Data AvailableYes
Raw Data File Type(s).cd,.cG, .xml, .bin,.stg
Uploaded File Size5.2 G
Analysis Type DetailGC/LC-MS
Release Date2015-03-13
Release Version1
Maureen Kachman Maureen Kachman
https://dx.doi.org/10.21228/M8359Z
ftp://www.metabolomicsworkbench.org/Studies/ application/zip

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Project:

Project ID:PR000219
Project DOI:doi: 10.21228/M8359Z
Project Title:Metabolic analysis of Parp1 ko/wt Saline & Bleo Mouse Lung Fibroblasts and Human IPF & Normal Lung Fibroblasts
Project Type:Glycolysis/TCA/Nucleotide analysis (tissue/cells)
Project Summary:Hedgehog signaling plays important roles in cell development and differentiation. In this study, the ability of Sonic Hedgehog (SHH) to induce myofibroblast differentiation was analyzed in isolated human lung fibroblasts, and its in vivo significance was evaluated in rodent bleomycin-induced pulmonary fibrosis. The results showed that SHH could induce myofibroblast differentiation in human lung fibroblasts in a Smo- and Gli1-dependent manner. Gel shift analysis, chromatin immunoprecipitation assay, and site-directed mutagenesis revealed that a Gli1 binding consensus in the ?-SMA gene promoter was important for mediating SHH-induced myofibroblast differentiation. Analysis of Hedgehog reemergence in vivo revealed that of all three Hedgehog isoforms, only SHH was significantly induced in bleomycin-injured lung along with Gli1. The induction of SHH was only noted in epithelial cells, and its expression was undetectable in lung fibroblasts or macrophages. Transforming growth factor (TGF)-? induced SHH significantly in cultured alveolar epithelial cells, whereas SHH induced TGF-? in lung fibroblasts. Pulmonary fibrosis and ?-smooth muscle actin (?-SMA) expression were significantly reduced in mice that were Smo deficient only in type I collagen–expressing cells. Thus, the reemergence of SHH in epithelial cells could result in induction of myofibroblast differentiation in a Smo-dependent manner and subsequent Gli1 activation of the ?-SMA promoter.
Institute:University of Michigan
Department:Deaprtment of Pathology
Laboratory:Sem H. Phan
Last Name:Hu
First Name:Biao
Address:Ann Arbor, MI
Email:biaohu@med.umich.edu
Phone:734-7635731
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