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Previously we showed that epidermal cells are able to use fibrinogen (FGN) as a migration substratum during wound closure. The goal of the present study was to determine the structural features of FGN that allow this migration. Pieces of glass coated with native, fragmented, or other modified forms of FGN were implanted into full-thickness skin wounds of adult newts such that migrating epidermal cells would encounter the implant. In this system, a coating of FGN allowed considerably more migration than a coating of BSA. At high concentrations, heat-denatured FGN supported as much migration as the same amount of intact FGN. Fraction I-9, a circulating form of FGN missing a 20-30K (K = 10(3) Mr) carboxy-terminal segment of the A alpha chain, was no less effective than intact FGN. Comparison of the isolated D1 and E fragments of FGN showed migration only on D1, but never to the extent seen on intact FGN containing the same amount of D1. Plasmin digestion of D1 in the presence of EDTA, a process which produces D3, a fragment differing from D1 by the loss of the carboxy-terminal 109 amino acids of the gamma chain, caused a significant loss of activity in the D fragment. Migration was good on implants coated with relatively high concentrations of purified A alpha chains but gamma chains were inactive. Migration over intact FGN was almost totally blocked by 230 microM-Arg-Gly-Asp-Ser (RGDS), a peptide known to interact with integrin-type receptors.(ABSTRACT TRUNCATED AT 250 WORDS)
The regenerative response of minced cardiac muscle grafts in the adult newt was studied using autoradiography and electron microscopy. One-sixteenth to one-eighth of the newt ventricle was amputated, minced, and returned to the wounded ventricle. At five days after grafting, no reorganization of graft msucle pieces was apparent and there was degeneration of much of the muscle graft. Another, smaller population of 5-day myocytes had euchromatic nuclei and intact sarcolemmae. In 10- and 16-day grafts, continuity between ventricular and graft lumina was established and coalescence of graft pieces was apparent. Ultrastructurally, 10- and 16-day graft myocytes appeared to have fewer myofibrillae and increased amounts of rough endoplasmic reticulum, polyribosomes, Golig complexes, and dense bodies when compared to uninjured ventricular myocytes. The peak of proliferative activity of graft cells was observed at 16 days. Electron microscopic autoradiography revealed breadkdown of myofibrillar structure in labeled myocytes, whereas in myocytes in the later stages of mitosis only scattered myofilaments and no Z bands were present. By 30 days, grafts appeared as an integrated structure composed primarily of cardiac muscle. Myocytes of 30-day grafts were observed in various stages of myofibrillogenesis and contained numberous 10-nm filaments. Seventy-day graft mycoytes had numberous well organized myofibrillae and intercellular junctions similar to those seen in uninjured ventricular myocytes.