Extracellular matrix cellular function

The secretion of extracellular matrix proteins is also a function of smooth muscle cells but, since it occurs concurrently with other activities, it does not seem to constitute a physiological state. However, the fraction of the cellular resources which are devoted to it must be regulated these regulatory mechanisms are virtually unknown. In addition, it should be anticipated that autocrine activity occurs as well, involving peptides, prostaglandins, cytokines, and nitric oxide. 

The MMPs are a family of zinc-dependent neutral endopep-tidases that share structural domains but differ in substrate specificity, cellular sources, and inductivity (Table I). All the MMPs are important for remodeling of the extra cellular matrix and share the following functional features (/) they degrade extracellular matrix components, including fibronectin, collagen, elastin, proteoglycans, and laminin, (//) they are secreted in a latent proform and require activation for proteolytic activity, (///) they contain zinc at their active site and need calcium for stability, (/V) they function at neutral pH, and (v) they are inhibited by specific tissue inhibitors of metalloproteinases (TIMPs). 

In every tissue of the body cells are cemented into place by a variety of proteins and proteoglycans which constitute the extracellular matrix (ECM). This protein mat provides a secure foundation for the cells, but its components also have effects on cell function and differentiation. Cellular attachment is mediated by a family of matrix receptors found on the cell surface called integrins. Integrins secure the cell to the matrix, and determine cell shape, migration and spread. 

Thyroid orbitopathy is an inflammatory disease of the orbital tissues. This inflammation is mediated through cytokine release, proliferation of fibroblasts, increased deposition of extracellular matrix, and adipocyte differentiation and proliferation. These cellular changes result in enlargement of the extraocular muscles and increased volume of orbital soft tissues, which presents clinically as exophthalmos and optic nerve compression. Edema, inflammation, and late fibrosis account for the decreased function of the extraocular muscles despite relative preservation of the muscle fibers themselves. 

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