Figure 2.

Model depicting relationship between mechanical tension, and collagen production and fragmentation in human skin. In sun-protected young adult human skin, intact type I collagen fibrils in the dermis provide mechanical stability and attachment sites for fibroblasts. Receptors (integrins) on the surface of fibroblasts attach to collagen (and other proteins in the dermal extracellular matrix). Cytoskeletal machinery (actin-myosin microfilaments, not shown) within fibroblasts pulls on the intact collagen matrix, which in turn offers mechanical resistance. Dynamic mechanical tension that is created promotes assembly of intracellular scaffolding (microtubules/intermediate filaments, not shown), which pushes outward to cause fibroblasts to stretch. This stretch is required for fibroblasts to produce normal levels of collagen and MMPs. In photodamaged/aged human skin, attachments of fibroblasts to integrins are lost, and fragmented collagen fibrils fail to provide sufficient mechanical stability to maintain normal mechanical tension. Reduced mechanical tension causes fibroblasts to collapse, and collapsed fibroblasts produce less procollagen and more collagenase (COLase). Reduced collagen production and increased collagenase-catalyzed collagen fragmentation result in further reduction of mechanical tension, thereby causing continual loss of collagen.