Hardie Lab

  • Current Projects

    The current projects in the laboratory include:

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    + Identification of specific cell signaling pathways which can be targeted alone or in combination to reverse progressive pulmonary fibrosis

    This project focuses on identifying cell signaling pathways which are downstream of epidermal growth factor receptor activation which mediate fibroproliferation. The goal is to identify specific pathways which can be pharmacologically targeted that not only prevent lung fibrosis progression, but augment reversal of existing fibrosis.

    Funding:
    NIH/NHLBI including RO1 and P50 grants.

    Collaborators:
    George Thomas, PhD
    University of Cincinnati
    Department of Cancer and Cell Biology

    + Identification of the sources of fibroblasts and mesenchymal cells which comprise and produce pathologic lung fibrosis

    The goal of this project is to determine the origin of cells which comprise lung fibrosis. A specific focus of this project is to determine the mechanisms and roles of cells originating from the bone marrow that are found in fibrotic lung lesions.

    Funding:
    American Heart Association- Grant to Dr. Madala

    + The role of TH-2 cytokines modulating inflammation and remodeling in the skin and lung

    This project examines the role of interleukin-31(IL-31) in mediating skin and lung fibrosis and the relationship of IL-31 with other TH-2 cytokines and receptors including IL-4 and IL-13.

    Funding:
    Bristol-Myers Squibb
    RO3 grant from the NIH – Pending

    + Mechanisms of fibrosis resolution and irreversible remodeling

    This project focuses on understanding the biology of how lung fibrosis resolves and the mechanisms whereby lung fibrosis becomes an irreversible scar.

    + Mechanisms of secondary pulmonary hypertension associated with pulmonary fibrosis

    Pulmonary hypertension is a significant co-morbid factor in patients with pulmonary fibrosis. This project examines the mechanism whereby fibrotic lung tissue leads to pulmonary hypertension and explores pharmacologic and genetic mechanisms to reduce pulmonary hypertension in the presence of persistent fibrosis.


  • These projects are designed to provide preclinical data to identify novel approaches for treating progressive fibrosis. Many of these projects utilize pharmacologic agents that are currently in advanced clinical trials for a number of diseases. Therefore, important findings could be relatively rapidly translated into clinical trials in patients with fibrotic disease.

  • lung biopsy
    image of schemata
    Trichrome stain.
    Hematoxylin and eosin stain.
    Cell signaling pathways.
    Smooth muscle actin stain.
    PI3K inhibition.
    Hematoxylin and eosin stain on lung sections from mice overexpressing TGFa.
    Representative photomicrographs of lung plural regions from TGFα mice.
    green florescent protein.