Collagen fibroblasts

THE MOLECULAR BASES OF THE CHONDRODYSPLASIAS INCLUDE MUTATIONS IN GENES ENCODING TYPE II COLLAGEN FIBROBLAST GROWTH FACTOR RECEPTORS... 

Cell-based products Collagen Fibroblasts and keratinocytes Venous ulcer treatment Eagistein et al., 1999... 

Fibroblasts (human foreskin) Rat tail tendon collagen Fibroblasts condense a hydrated collagen lattice Bell etal. (1979)... 

In the interstitium, angiotensin II induces proliferation of mesangial cells and fibroblasts and the synthesis of collagen and other matrix molecules by these cells via the ATI receptor. Moreover, by the concomitant stimulation of chemoattractant cytokines, inflammation is induced. These processes are mediated by endothelin, transforming growth factor(3, and reactive oxygen species, and finally lead to interstitial fibrosis and glomerulosclerosis observed in hypertension and diabetes. 

The in vitro biocompatibihty of wound dressings in regards to fibroblasts has been assessed and compared with three commercial wound dressings made of collagen, alginate and gelatin. Methylpyrrolidinone chitosan and collagen were found to be the most compatible materials [305,306],... 

Nagata, K., Saga, S. Yamada, K.M. (1986). A major collagen-binding protein of chick embryo fibroblasts is a novel heat shock protein. Journal of Cell Biology, 103, 223-9. 

Moy LS, Howe K, Moy RL (1996) Glycolic acid modulation of collagen production in human skin fibroblast cultures in vitro. Dermatol Surg 22(5) 439-441... 

The ability of these peptidomimetic collagen-structures to adopt triple helices portends the development of highly stable biocompatible materials with collagenlike properties. For instance, it has been found that surface-immobilized (Gly-Pro-Meu)io-Gly-Pro-NH2 in its triple-helix conformation stimulated attachment and growth of epithelial cells and fibroblasts in vitro [77]. As a result, one can easily foresee future implementations of biostable collagen mimics such as these, in tissue engineering and for the fabrication of biomedical devices. 

Chojkier, M., Houghim, K., Solis-Hemizo, J. and Brenner, D.A. (1989). Stimulation of collagen gene expression by ascorbic acid in cultured human fibroblasts A role for lipid peroxidation J. Biol. Chem. 264, 16957-16962. 

Min DJ, Cho ML, Lee SH, et al. Augmented production of chemokines by the interaction of type II collagen-reactive T cells with rheumatoid synovial fibroblasts. Arthritis Rheum 2004 50(4) 1146-1155. 

Recently, the notion that the chronicity of inflammation may not actually drive the fibrogenic process has been widely appreciated (Tables 1, 2, and 3). Some propose that it is indeed the alteration of the mesenchymal cell phenotypes that disrupts the balance between collagen synthesis and degradation in the wound-healing process, highlighted by clinical evidence that shows unsuccessful treatment of fibrosis with anti-inflammatory or immunosuppressive drugs (18,19). One scenario is that mesenchymal cells (myofibroblasts and fibroblasts) are phenotypically altered and thus do not undergo apoptosis after resolution. 

Inhibition of IFN-y entails inhibition of fibroblast proliferation and differentiation, subsequent collagen synthesis, and increased expression of MMP-1 to promote degradation of matrix (105). IFN-y also triggers robust T-lymphocyte... 

Gharaee-Kermani M, Denholm EM, Phan SH. Costimulation of fibroblast collagen and transforming growth factor betal gene expression by monocyte chemoattractant protein-1 via specific receptors. J Biol Chem 1996 271(30) 17779-17784. 

Fig. 14.1. The Thl/Th2 balance is central to the regulation of normal wound repair. Tissue injury results in the initiation of an inflammatory response, mediated by a variety of cells and their by-products. Immune cells are recruited and cross-regulate the Thl/ Th2 balance that occurs in response to the cytokine environment. This balance is in turn cross-regulated by the chemokine/chemokine-receptor expression profile, which functions to amplify the inflammatory process. Cells residing in the injured tissue release profibrotic mediators, which promote fibroblast activation, proliferation, and differentiation to the myofibroblast phenotype. Myofibroblasts produce collagen to repair damaged tissue, which is an event that is favored by the inhibition of MMP activity. The Thl/Th2 balance is central to whether a normal or aberrant wound-repair process is established A Thl environment promotes normal tissue resolution (fibrinolysis), whereas a Th2 environment maintains the progression of fibrotic disease (excessive collagen deposition).

Fig. 20. hypothetical mode of action of melampolides on skin. C, collagen F, fibroblast GS, ground substance EL, elastine. 

The thickness of the blood-gas interface is normally less than 0.5 (im. This extremely thin barrier promotes the diffusion of gases. The thickness may increase, however, under conditions of interstitial fibrosis, interstitial edema, and pneumonia. Fibrosis involves the excess production of collagen fibers by fibroblasts in the interstitial space. Edema is the movement of fluid from the capillaries into the interstitial space. Pneumonia causes inflammation and alveolar flooding. In each case, the thickness of the barrier between the air and the blood is increased and diffusion is impaired. 

Haehling, E., Niederkorn, J.Y. and Stewart, G.L. (1995) Trichinella spiralis and Trichinella pseudospiralis induce collagen synthesis by host fibroblasts in vitro and in vivo. InternationalJournal of Parasitology 25, 1393—1400. 

Grinnell F (2003) Fibroblast biology in three-dimensional collagen matrices. Trends Cell Biol... 

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