Our lab primarily studies the extracellular matrix (ECM) and its roles in tissue remodeling, nutrient homeostasis, and smooth muscle function. We have several different areas of investigative emphasis including but not limited to:

  1. Cell-mediated collagen turnover pathways in tissue fibrosis
  2. Fatty acid uptake and how this relates to disease states such as insulin resistance and obesity
  3. Tissue inflammation and cellular proliferation in both airway and vascular smooth muscle

Specific projects currently being pursued in the lab are as follows:

  1. Investigating cell-mediated collagen uptake and degradation pathways in the context of tissue fibrosis. We previously reported that macrophage-mediated resorption of fibrillar collagens is crucial in limiting the severity of fibrosis and are applying functional genomics approaches to further explore this observation. Our ultimate goal is to identify novel therapeutic targets that, when targeted, could potentially reverse established fibrosis.
  2. Understanding the extracellular pathways that control absorption of glucose, dietary fats and how these nutrients are metabolized and/or deposited in peripheral stores. We are particularly interested in exploring the link between fatty acids and insulin resistance.
  3. Inhibiting activation of RhoA to prevent bronchoconstriction. Airway constriction is the main cause of shortness of breath in asthma and occurs in large part due to an increase in calcium sensitivity induced by allergic inflammation of airway smooth muscle. We previously identified a pathway that inhibits the ability of cytokines released in the asthmatic airway to increase calcium sensitivity and are now investigating the upstream mediators of this effect.