Connective tissue remodeling

Parodi, RE. et al.. Oral administration of diferuloylmethane (curcumin) suppresses proinflammatory cytokines and destructive connective tissue remodeling in experimental abdominal aortic aneurysms, Ann. Vase. Surg., 20, 360, 2006. 

Tomasek, J.J., Gabbiani, G., Hinz, B., Chaponnier, C., and Brown, R.A. 2002. Myofibroblasts and mechano-regulation of connective tissue remodelling. Nat. Rev. Mol. Cell Biol. 3 349-363. 

Woessner, J.F. (1991). Matrix metalloproteases and their inhibitors in connective tissue remodeling. FASEBJ. 5 2145-2154. 

MMP-9 is preferentially expressed in UIP (46). The concentrations of MMP-9 and tissue inhibitors of metalloproteinases (TIMPs) are more increased in BAL fluid of patients with OP than in those with UIP (47). These data suggest that an imbalance between MMPs and TIMPs may play a role in the connective tissue remodeling of OP. Laminin-5, a glycoprotein involved in cell attachment, migration, proliferation, differentiation, and apoptosis expressed in epithelial cells of wound healing, is also expressed in regenerating epithelial cells in OP and UIP (48). 

The most important reaction requiring ascorbate as a cofactor is the hydroxylation of proline residues in collagen. Vitamin C is, therefore, required for the maintenance of normal connective tissue as well as for wound healing since synthesis of connective tissue is the first event in wound tissue remodeling. 

Tissue remodelling in normal healthy tissue is dependent upon continuous turnover of connective tissue elements. This requires dissolution of structural matrix proteins, and laying down of new structural components. Acute... 

Taken together, the identification of mast cell hyperplasia and mediator release at sites of tissue fibrosis and wound healing, observations in animal models, and study of the actions of mast cell products, has provided much circumstantial evidence that mast cells are involved in tissue remodelling, healing and fibrosis. It is unlikely that mast cells are essential in these responses, but more likely that they augment them. Complex interactions between different connective tissue components, mast cells and other inflammatory cells are likely to operate, and are unlikely to be fully delineated in humans in vivo. It seems reasonable to hypothesize however that initial mast cell mediator release has the potential to activate fibroblasts, which may then promote the recruitment at d proliferation of further mast cells, explaining the mast cell hyperplasia often witnessed at sites of chronic inflammation. 

Kuhn, C., Boldt, J., King, T.E.Jr. et al. (1989). An immuno-histochemical study of architectural remodeling and connective tissue synthesis in pulmonary fibrosis. Am. Rev. Respir. Dis. 140, 1693-1703. 

Many cells secrete at least one of the three immature forms of TGF-P, and essentially all cells have receptors that respond to the presence of mature TGF-P in the stroma. In the periodontium, TGF-P stimulates fibroblast and osteoblast proliferation during connective tissue or bone remodeling (Sect. 10.1.3), and maintains the proliferation of dentally attached epithelial cells (Sect. 5.2.3). The linker domains that connect calcium binding domains in fibrillin are identical to the sequence of protein receptors that bind to TGF-P (Sect. 6.1.1). 

Intramembranous ossification is responsible for most of the mineralization of the skull, including the maxilla and mandible. It begins with the differentiation and activation of osteoblasts from fibroblast-related precursors within a region of connective tissue that demarcates where the bone will develop. The osteoblasts secrete a nonmineralized protein-rich (osteoid) matrix and, as they move away, the matrix mineralizes (Fig. 9.3a). The periosteum remains uncalcified and contains latent and undifferentiated osteoblasts for bone remodeling. Odontoblasts (Ob) and cementoblasts secrete an osteoid-like matrix similar to that of intramembraneous ossification. 

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