The glycosaminoglycans of open wounds

Hyaluronate activation of CD44 induces insulin-like growth factor-1 expression by a tumor necrosis factor-alpha-dependent mechanism in murine macrophages.

“…Increased amounts of hyaluronic acid have been demonstrated in several animal models of inflammatory tissue injury as well as disease states such as pulmonary fibrosis (14)(15)(16). Increased production of hyaluronic acid is an early event in connective tissue reparative processes associated with wound healing (53,54). Since hyaluronate is also a constituent of the normal extracellular matrix, as well as being present in large quantities in synovial fluid, there must be a mechanism preventing chronic activation of inflammatory cells.…”

Hyaluronan and Rat Renal Fibroblasts: In vitro Studies

“…There is increasing evidence to show the correlation of an increased but transient production of HA with rapid cell migration during processes such as inflammation [6, 7, 8, 30], wound repair [29], and morphogenesis of a variety of tissues [2, 3]. This HA is later degraded by fibroblasts during the healing phase of inflammation at a time when synthesis of sulfated glycosaminoglycans is increasing [1]. Where injury is destructive, recession of HA is followed by the development of a scar in which collagenous tissue replaces the parenchymal cells and their normal matrix, then condenses and contracts [1].…”

“…The immediate biological response to tissue injury is local inflammation, followed by cell proliferation and deposition of both collagenous and noncollagenous matrix components. The latter components include the class of molecules called glycosaminoglycans, a diverse group of molecules widely distributed in animal tissues and produced by most animal cells [1]. One of the glycosaminoglycans involved in these processes is hyaluronic acid or hyaluronan (HA).…”

“…This macromolecule is important in several physiological and pathological processes and is present at high concentrations in tissues undergoing remodelling and morphogenesis where it acts as a support for cell adhesion and locomotion [1, 2, 3]. …”

Stimulation of glycosaminoglycan synthesis in cultured human dermal fibroblasts by interleukin 1. Induction of hyaluronic acid synthesis by natural and recombinant interleukin 1s and synthetic interleukin 1 beta peptide 163-171.

“…HA is synthesized early during the course of an inflammatory reaction and is later degraded by fibroblasts during the healing phase of inflammation at a time when synthesis of sulfated glycosaminoglycans (GAGs) is increasing (7). Mechanisms involved in controlling this resynthesis ofGAGs are not completely understood.…”