Connective tissue components

Several of these morphological factors are illustrated in Figure 1. Figure lA is of the fat portion of bacon and has been stained for connective tissue. It is noted that fat tissue is not all lipid but has an extensive connective tissue component ranging from fairly thick layers to delicate layers defining each adipose cell. Figure IB is from a finely chopped emulsion. Connective tissue pieces are stained dark, the protein matrix is gray and the... 

Human leukocyte elastase is a protease that degrades elastin and other connective tissue components. It is implicated in the pathogenesis of pulmonary emphysema and other inflammatory diseases such as rheumatoid arthritis and cystic fibrosis. Porcine pancreatic elastase has often been used as a model for HLE. Both enzymes have a small primary binding site Si. 

Binding of Lp(a) to fibronectin, a connective tissue component in atherosclerotic plaques, when considered in adjunct to the former observations, supports the hypothesis that Lp(a), just like LDL, is transported through endothelium, and subsequently immobilized in the arterial intima by binding of matrix components (V6a). The particle then possibly undergoes oxidative modification, is taken up by macrophages, and therefore contributes to foam cell formation and atherogenesis (SI). 

Table 1.1. Location and composition of connective tissue components...

Leukocytes, macrophages, and mast cells are observed at one stage or another of most inflammatory diseases. All of these cells are rich in proteases and are important mediators of allergic, infective, and anaphylactic reactions of tissues in most animals. It is likely that proteases released from these cells contribute to the inflammatory process by degrading connective tissue components and by releasing kinins. 

Other studies have shown that other connective tissue components, including cartilage proteoglycan and collagen, are susceptible to ROI-dependent injury. Fragmentation of proteoglycan after exposure to HO -generating systems is well... 

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. 

PMN Products - Neutral proteinases of PMN lysosomes degrade a wide variety of collective tissue substrates including elastin, proteoglycan, and collagen. Cathepsin G has been found only in PMN, and elastase from these cells has a substrate gpecificity different from that of pancreatic and macrophage elastase. In addition to their effects on connective tissue components, the neutral proteinases of PMN lysosomes also stimulate the activity of other cells involved in the inflammatory response. Both elastase and cathepsin G from human PMN stimulate the incor- poration of thymidine by human peripheral blood and splenic lymphocytes. The stimulated lymphocytes are of the B lineage, with no effect seen on T lymphocytes. 

A characteristic but unexplained feature of the peptide composition of all of these glycopeptides and peptido-oligosaccharides (see Table V) is the absence, or presence in traces only, of the aromatic amino acids. The presence of hydroxy-L-proline in some of these fractions might indicate that the glycopeptide components of these fractions are derived from connective-tissue components, as this... 

The connective-tissue components collagen and elastin are the probable source of some urinary protein-carbohydrate compounds. A glycopeptide containing approximately equimolar proportions of hy-droxy-L-lysine, D-glucose, and D-galactose has been isolated from... 

Maintenance and repair of duodenal and gastric collagen and elastin connective tissue components also seems to be an important copper-dependent enzyme function in preventing or repairing duodenal or gastric ulcers. Induction or facilitation of de novo synthesis of lysyl oxidase by copper complexes [16] merits consideration to account for the observed rapid and normal replacement of connective tissue components in the surgically placed gastric ulcer model [178]. 

Histologically visible fibers of collagenous nature are complex objects (see Fig. 1). They may, on occasion, be expected to show chemical and physical properties characteristic of any of the major connective tissue components, even though they may most often resemble collagen predominantly. 

Studies on the mechanical behavior of the mitral leaflet tissue have been conducted to determine the key connective tissue components which influence the valve function. Histological studies have shown that the tissue is composed of three layers which can be identified by differences in ceUularity and collagen density. Analysis of the leaflets under tension indicated that the anterior leaflet would be more capable of supporting larger tensile loads than the posterior leaflet. The differences between the mechanical properties between the two leaflets may require different material selection for repair or replacement of the individual leaflets [Kunzehnan et al., 1993a,b]. 

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