Modeling Extracellular Matrix-Cell Interactions in Lung Repair and Chronic Disease

Dear Colleagues,

The extracellular matrix (ECM) provides tissue architecture in the lung by providing mechanical stability and elastic recoil, which are essential for normal lung physiology. In addition to biomechanical signals through ECM-cell attachment, the lung ECM also directs cell functions through its biochemical composition and reservoir function for several growth factors and cytokines. ECM-cell interactions within the lung are essential for cell proliferation, differentiation, motility, cell–cell communication, and survival and are, therefore, essential in the mechanisms of tissue inflammation and repair. The progression of several chronic lung diseases including asthma, chronic obstructive pulmonary disease (COPD), interstitial pulmonary fibrosis (IPF), and acute respiratory distress syndrome (ARDS) have been associated with alterations in lung ECM–cell interactions. The ECM is a complex mixture of fibrous proteins that provide tensile strength (collagen, elastin), adhesive glycoproteins (fibronectin, laminin), and glycosaminoglycans and the proteoglycans (heparin, chondroitin sulfate) that resist compressive forces. The lung ECM is organized into two main structural types: 1) basement membranes, which are thin, dense sheets of specialized, self-assembled ECM proteins that sit between epithelial tissues (including mesothelium and endothelium), and the underlying connective tissue; which consists of 2) an interstitial matrix that is formed of a porous ECM that forms a 3-dimensionl lattice around cells. A recent proteomics study on the mouse lung ECM demonstrated over 150 different ECM proteins, glycosaminoglycans, and modifying enzymes. In recent years, the use of 3-dimensional tissue engineered in vitro model systems such as air–liquid interface cultures, lung organoids, precision-cut lung slices, lung-on-a-chip models, ECM gels, and co-culture systems, as well as animal studies have been used to model the complex cell–cell–ECM interactions within the lung. The primary focus of this Special Issue will be an exploration of how different disease models are elucidating ECM repair mechanisms in healthy and chronically diseased lungs. The reviews and research articles will assess the contribution of different cytokine and growth factor signaling pathways, gene regulation, epigenetic mechanisms, biomechanical signaling to cell-EM repair responses through a myriad of disease-relevant models.

Prof. Tillie-Louise Hackett
Dr. Emmanuel Twumasi Osei
Guest Editors

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