The fine structure of fibroblasts in thin sections was studied with the electron microscope in an attempt to determine the site of collagen synthesis and the mechanism of extrusion of collagen precursors. Use was made of the skin of embryonic, newborn and adult mice, and the granulation tissue in the healing of skin wound of mice. Actively functioning fibroblasts were characterized by a well developed endoplasmic reticulum, enlarged Gologi complex and swollen mitochondria. Some filamentous dense materials, presumably collagen precursors, were found within the cisternae of the endoplasmic reticulum and in the peripheral region of the cytoplasm. The newly formed collagen fibrils were found in contact with the cell surface. They developed into mature form in the extracellular spaces. This study emphasized that collagen precursors are produced in close association with the endoplasmic reticulum and sythesized products are accumulated within distended cisternae of of the reticulum and discharged from the cell by perforating the cell surface or through separation of the whole cisternae from the cytoplasm.
Effect of various substances upon the reconstitution of fibrils in vitro from dissolved collagen was also studied with the electron microscope. The results support the view that polymerization of collagen precursors, extruded from the cells may occur through a physicochemical effect of extracellular fluids, possibly with the aid of mucopolysaccharides in the grown substance.
The structural changes of the fibroblasts were observed in some pathological conditions, including human laryngeal nodules, wound healing in scorbutic guinea-pigs and in mice injected with cortisone. The fibroblasts in the laryngeal nodules showed a failure of the development of the endoplasmic reticulum and abundant cytoplasmic filaments, possibly collagen precursors accumulated in the cell matrix instead of within the lumen of the endoplasmic reticulum associated with less abundant RNP particles on the outer surface. Cortisone injection resulted in a striking depression of the proliferation of the fibroblasts, which contained a poorly developed endoplasmic reticulum and many inclusion bodies in the cytoplasm. The possible mechanism of the disturbance of collagen production in these pathological conditions was discussed in the light of the knowledge of fibrogenesis in connective tissue.
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