Читать книгу Musculoskeletal Disorders - Sean Gallagher - Страница 85

Tenocytes are stellate in shape when examined in longitudinal sections, with elongated protrusions in all directions. These protrusions contact tenocytes within the same and adjacent rows, thus forming an intricate tendon network. There are gap junctions at these contact points. Gap junction proteins, such as, connexin 43, are expressed at these sites and are thought to regulate the transfer of proteins between tenocytes via mechanisms that are still unclear. Yet, these gap junctions are considered essential mediators of the mechanotransduction function of tenocytes (mechanotransduction is defined as a cell’s response to mechanical cues by biochemical signals). Similar to other mechanosensitive cells, mechanotransductive responses are involved in tenoctye homeostasis, healing, and degeneration. Tenocyte homeostasis is regulated by the production of degradative enzymes (e.g., matrix metalloproteinases [MMPs]) and extracellular proteins (e.g., collagen). Altered mechanical loading promotes changes in mechanosensitive proteins, including integrins and the tenocyte transcription factor, scleraxis, which is important for tenogenesis. Altered mechanical loading also leads to increased production of transforming growth factor beta 1 (TGFbeta‐1). TGFbeta‐1 is a key regulator of differentiation, proliferation, and extracellular matrix production for most cell types, including tenocytes. The production of several other proteins is altered by mechanical loading, including the cytokine IL‐1, cyclooxygenase 2 (COX2), platelet‐derived growth factor (PDGF), and CCN2/CTGF (cell communication network factor 2, formally known as connective tissue growth factor). In this manner, altered mechanical loading can lead to catabolism (via a degradative environment) or anabolism (increased tenocyte biomechanical properties via altered production in the mix of extracellular matrix proteins).