APS Annual Meeting at Experimental Biology



Tissue Remodelling and Fibrosis in the Gastrointestinal Tract - The Regulation of Matrix Deposition, Mesenchymal Cell Expansion, and the Impact of the Microbiota

Symposium — Thursday, April 29, 2021 — 2:00 PM - 3:30 PM — , Room APS-9
GI and Liver Physiology Section — Chair: Simon Hirota — Co-Chair: Amy C Engevik

Following injury in the gastrointestinal tract, reparative fibrogenic responses trigger mesenchymal cell activation/proliferation, tissue matrix production and remodelling; processes that are usually self-limiting processes. However, in the context of exaggerated injury or chronic inflammation, sustained activation of mesenchymal cells and fibrogenesis leads to pathogenic tissue remodelling and contributes to organ dysfunction.  As a result, fibrosis is a common and potentially serious complication of a number of gastrointestinal disorders, including inflammatory bowel diseases (IBD) and non-alcoholic steatohepatitis (NASH). The mechanisms contributing to aberrant tissue remodelling involve multiple cell types and interconnected cell signaling events. Furthermore, there is a growing body of data outlining host-microbe interactions as a key regulator of fibrogenesis. This session will outline some of the key cellular and molecular events that contribute to tissue repair and, when dysregulated, drive pathogenic tissue remodelling in the liver and intestine. The overarching objective of this symposium will be to provide an integrated perspective on the role of mesenchymal cells and host-microbe interactions in tissue repair and pathogenic remodelling, which is a growing field in gastrointestinal physiology.

Speakers

  • The dynamics of matrix remodelling and fibrosis in liver injury
    Natalia Nieto — Pathology, University of Illinois at Chicago

  • Microbial regulation of intestinal fibrosis – dissecting the role of siderophores
    Janelle C Arthur — Microbiology & Immunology, University of North Carolina

  • Epigenetic regulation of intestinal smooth muscle in the pathogenesis of fibrostenosis
    Michael Blennerhassett — Medicine, Queen’s University




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