ISSN:
1524-475X
Quelle:
Blackwell Publishing Journal Backfiles 1879-2005
Thema:
Medizin
Notizen:
Hypertrophic scars are a resultant of a fibroproliferative disorder observed at the time of the wound healing of large surface, like burns. In normal wound, the process of healing begins with the invasion in the wound of microvascular cells and by the migration of myofibroblasts to form the granulation tissue. There, myofibroblasts play an important role since they synthesize the extracellular matrix and are responsible for the contraction of the wound. At the end of the healing process, the myofibroblasts disappear by apoptosis via unknown stimuli. In the case of hypertrophics scars, there is persistence of a high density of cells and collagen in comparison with normal granulation tissue. Scientists associate this disorder with a problem in the regulation of apoptosis. Our hypothesis is that endothelial cells play an important role in the persistence of myofibroblasts in wound healing. We have compared the apoptotic rates of human myofibroblasts from normal wounds (Wmyo) with those from hypertrophic scars (Hmyo) when exposed with supernatants from microvascular cells isolated from normal skins (CEMV) or hypertrophic scars (CEMVH). The first results showed a significative reduction of apoptosis for Hmyo while Wmyo were not found to respond to the microvascular supernatant. There were, however, no difference in the apoptotic rates of both populations of cells when exposed to CEMV or CEMVH supernatants. These results suggest that endothelial cells secrete one or many factors that inhibit Hmyo apoptosis, thus preventing the disappearance of those cells and inducing the formation of hypertrophic scars. We hope that a better understanding of the mechanisms implicated in the formation of hypertrophic scars will open the way to new treatments.Acknowledgments: This research was granted by CIHR and the Fondation of the HSS of CHA VM was recipient of scholarships from Centre de Recherche du CHA-FRSQ and FRSQ.
Materialart:
Digitale Medien
URL:
http://dx.doi.org/10.1111/j.1067-1927.2005.130216x.x
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