Colonic organogenesis in rats was studied using light microscopic techniques for the demonstration of mucosubstances, glycogen, and connective tissue fibers. Crypts began as intraepithelial spaces which were in continuity with the colonic lumen. The cells forming the floors of these invaded the nonsulfated acid glycosaminoglycan-rich mesenchyme as the basement membrane became discontinuous. As the diameter of the colon increased, the crypts lengthened and the lamina propria thickened until a layer of collagen and sulfated acid glycosaminoglycans formed at the bases of the crypts and the basement membrane was reestablished. The circular layer of the muscularis externa developed first, then the longitudinal layer, and finally the muscularis mucosae. Three types of mucous cells arose in these newly formed crypts. The initial epithelial cell type contained glycogen and gave rise to cells with apical coats of nonsulfated acid glycoproteins. This cell type was followed by the appearance of cells at the bases of the crypts containing nonsulfated acid glycoproteins. As the crypts lengthened, the goblet cells near the base contained nonsulfated and/or sulfated acid glycoproteins. Closer to and on the surface, the cells contained sulfated acid glycoproteins, a mixture of sulfated acid and neutral glycoproteins, or just neutral glycoproteins. Striated-border cells appeared intermingled with the mucous cells close to the bases of the crypts and continued onto the surface. A comparison was made between regeneration following placement of a surgical lesion in adult rats and events in organogenesis of the colon.
2841 C1) and the Upjohn Company. 2Based on a dissertation submitted in partial fulfillment of the requirements for the Doctor of Philosophy degree. 3 This investigation was carried out during the tenure of a Predoctoral Fellowship from the National Cancer Institute, United States Public Health Service. Deep appreciation is extended to Dr. Burton L. Baker for his direction of this investigation.
Hypertrophic scar tissue has been observed to soften and thin following Z plasty without removal of any of the scar tissue. Histochemical studies of tissue before and after Z plasty showed that abnormally sulfated mucopolysaccharides were replaced by normal acid mucopolysaccahrides within 14 days. Collagen in hypertrophic scar appeared in nodules and fibers perpendicular to the surface of the skin rather than as long straight fibers parallel to the skin surface as normally seen. Elastic fibers were reduced and scar was relatively avascular. Following Z plasty the amount of collagen decreased and fibers were oriented in bundles at right angles to each other, parallel to the surface. When tissue was examined by electron microscopy collagen fibers showed marked variation in diameter. Microfibrils were increased and there were aggregates of fibrils with periodicity of 1500 to 1600 A. Following Z plasty, areas which previously contained only microfibrils now had unit collagen fibers with normal periodicity. Urinary excretions of hydroxyproline and hydroxylysine, amino acids found only in collagen, were increased following Z plasty, coinciding with the softening of the scar. Excretion of the disaccharide, glucosylgalactosylhydroxylysine, predominantly found in skin, increased following Z plasty, while excretion of the monosaccharide, galactosyl-hydroxylysine, predominant in bone collagen, remained constant. Amino acid composition of collagen, remained constant. Amino acid composition of collagen isolated from hypertrophic scars was similar to that present in skin and tendon, and unlike that in cartilage or infant dermis. Hydroxyproline content was slightly decreased and hydroxylysine content slightly increased compared to skin or tendon. Histochemical, ultrastructural and biochemical studies of the same specimens suggested that collagen with disordered fibril formation was present in the hypertrophic scar and was degraded following Z plasty. Changes in the molecule which occurred after synthesis of the protein core might be responsible both for the failure of normal maturation of the scar and for its sensitivity to degradative enzymes following Z plasty.
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