Extracellular Matrix and Adhesion Molecules
The extracellular matrix provides the physical microenvironment in which cells exist. It provides a substrate for cell anchorage, serves as a tissue scaffold, guides cell migration during embryonic development and wound repair, and has a key roles in tissue morphogenesis. The extracellular matrix is also responsible for transmitting environmental signals to cells, which ultimately affects cell proliferation, differentiation and death.
Products for Extracellular Matrix and Adhesion Molecules
Extracellular Matrix Components
The extracellular matrix has three major components:
- Highly viscous proteoglycans (heparan sulfate, keratan sulfate, chondroitin sulfate), which cushion cells
- Insoluble collagen fibers, which provide strength and resilience
- Soluble multiadhesive extracellular matrix proteins (fibronectin, laminin), which bind proteoglycans and collagen fibers to receptors on the cell surface
Different combinations of these components tailor the matrix for different functions depending on the amount of strength (for example tendons), cushioning (for example cartilage) and adhesion required. All extracellular matrix components are synthesized intracellularly and secreted via exocytosis.
Cell adhesion molecules (CAMs) are involved in cell-cell and cell-extracellular matrix binding. The major classes of cell adhesion molecules are the integrins, cadherins, selectins and the immunoglobulin superfamily (N-CAM, ICAM, VCAM etc). In addition to their adhesive functions, cell adhesion molecules modulate signal transduction pathways by interacting with molecules such as receptor tyrosine kinases, Rho-GTPase and components of the Wnt signaling pathway.
ECM and Disease
Degradation of the extracellular matrix is required for the tissue remodeling associated with various physiological and pathological processes such as morphogenesis, angiogenesis, tissue repair, cirrhosis, arthritis and metastasis. Matrix metalloproteases are the major proteases involved in extracellular matrix degradation.
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November 15 - 19, 2014
Washington D.C., USA