Melatonin-induced augmentation of collagen deposition in cultures of fibroblasts and myofibroblasts is blocked by luzindole--a melatonin membrane receptors inhibitor.

BACKGROUND: Melatonin has been proven to have a regulatory influence on collagen accumulation in different types of wound. It was found to inhibit collagen accumulation in the superficial wound model but increase it in the myocardial infarction scar. The aim of the study is to determine the mechanism of melatonin action in the two wound types in rats.
METHODS: Cells were isolated from both the superficial wound (subcutaneously inserted polypropylene net) and myocardial infarction scar (induced by ligation of the left coronary artery) and were identified by electron microscopy.
RESULTS: Long-shaped cells forming whirl-like structures in culture (mainly identified as fibroblasts) were isolated from the superficial wound model, while myofibroblasts growing in a formless manner were acquired from the infarcted heart scar. Melatonin (10(-7) M) increased collagen accumulation in both fibroblast and myofibroblast cultures. Luzindole (10(-6) M), the blocker of both MT1 and MT2 melatonin membrane receptors, inhibited the effect of melatonin on the two types of cells.
CONCLUSION: Regardless of various healing potentials demonstrated by the tested cells (different cell composition, growth and organization), their response to melatonin was similar. Moreover, in the two investigated cultures, augmentation of the collagen content by melatonin was reversed by luzindole, which indicates the possibility of melatonin membrane receptor involvement in that process. The present results suggest that the increased melatonin-stimulated deposition of collagen observed in the infarcted heart of rats could be dependent on activation of the melatonin membrane receptors on scar myofibroblasts.