Tenocytes are the major cell type found in tendon; they are responsible for the synthesis and maintenance of collagen and other components of the extracellular matrix, and thus the structural integrity of tendon.
The keloid phenotype persisted in culture as demonstrated by the maintenance of collagen I and III expression, immune cell fraction (T cells, B cells, NK cells, mast cells, neutrophils, Langerhans cells), mesenchymal cells and endothelial cells.
Evidence suggests that maintenance of collagen matrix organization, inflammatory response, cellular mediators, expression of specific genes, and contribution of stem cells seem to be essential for tissue recovery [ 11].
However, if this phenomenon, of an initial burst of ECM generation that is then maintained resulting in chronic lung fibrosis, applies to IPF, future anti-fibrotic therapies should aim to target the maintenance of collagen and not the initial synthesis.
This study presents evidence of several novel regulatory functions of MATN3, including induction of IL-1Ra expression, maintenance of collagen II and aggrecan gene expression, and inhibition of the IL-1β-induced gene expression of certain catabolic matrix proteases including ADAMTS-5.
Indeed, fibrocartilaginous explants cultured in the presence of GM6001 showed an inhibition of relaxin-induced and β-estradiol plus relaxin-induced collagenase and stromelysin activities to control baseline levels that were accompanied by the maintenance of collagen or GAG content at control levels.
The antifibrotic role was observed by a reduction of soluble and tissue collagen, α-SMA accumulation around the granulomas 69 days post infection and the maintenance of soluble collagen levels between 48 and 69 days post infection.
Rapid fabrication of multilayer tubular conduits with maintenance of native collagen ultrastructure was achieved with internal diameters ranging between 1 and 4 mm.
These data provide evidence of altered anabolic activity within tendon in response to mechanical stimuli, and suggest the importance of cyclic tensile loading for the maintenance of the collagen hierarchy within tendon.
Normal skin architecture is dependent both on the coordinated proliferation and stratification of keratinocytes, as well as the maintenance of a collagen-rich basement membrane.
L-Sox5, Sox6 and Sox9 are necessary regulators for induction and maintenance of cartilage-specific collagen expression by chondrocytes [ 2].
