Our study revealed that as observed with both light and electron microscopy the most specific abnormality in sclerodermna skin is the replacement of the subcutaneous tissue by markedly abnormal connective tissue.
Intralobar instillation of cadmium chloride (CdCl2) into the left lungs of rats initiated a sequence of events that culminated in massive unilateral intraluminal fibrosis. Early events (days 1 and 2) after CdCl2 administration included infiltration of the treated lung with polymorphonuclear leukocytes, an increase in the number of alveolar macrophages, activation of the macrophages as assessed by the induction of cathepsin L mRNA, and the induction in liver of mRNA for the acute-phase response protein, alpha 1-acid glycoprotein. By days 5 to 7 in the treated lungs, mRNA for procollagen alpha 1(I) increased 20- to 60-fold, and mRNA for procollagen alpha 1(III) increased 4- to 14-fold. These increases were correlated with the almost complete filling of the alveolar spaces with fibroblasts and collagen. The contralateral lung exhibited no significant change in histology but showed a similar induction of collagen gene expression. These increases were tissue-specific, as the livers of these animals showed no change from the control levels of collagen gene expression. Procollagen messages in the treated and contralateral lungs were equally competent for translation into pro-alpha 1(I) and pro-alpha 2(I) polypeptides. Both the treated and contralateral lungs increased hydroxyproline content about 1.5- to 2-fold over 14 days. The contralateral lung, but not the treated lung, showed a 2-fold increase in lung volume. As a result, the collagen density (mg collagen/ml lung volume) doubled in the treated lung but remained constant in the contralateral lung. These data indicate that CdCl2 caused a rapid induction of pulmonary fibrosis in the treated lungs of rats and stimulated histologically normal growth of the contralateral lung.
Embryonic chick and hamster aortas were examined in the electron microscope using ferritin-conjugated, elastin-specific antibodies after etching of the plastic, thin sections with a dilute solution of benzene, methanol and ethanol. Specific staining of intracellular vesicles was observed in both smooth muscle and endothelial cells in addition to extracellular elastin fibers. In the chick cells, these ferritin-stained vesicles had a lipid-laden appearance. In both species the vesicles appeared to fuse with the plasma membrane and discharge their contents into the extracellular space suggesting elastin is secreted via vesicular structures.
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