ABSTRACT
In extensive burns it becomes difficult for fibroblasts to migrate from the periphery of the healthy tissue and colonize the injured area. Even under such circumstances healing takes place, and this is attributed to the differentiation of circulating fibrocytes which enter the wound site. This normal cell type is identified in keloid fibroblasts: it expresses fibrocyte markers and secretes extra cellular matrix proteins. In-vitro collagen contraction assay reveals that fibrocytes contract collagen gels with an efficacy similar to normal fibroblasts. The contribution of fibrocytes to the formation of keloid fibroblasts in post-burn healing is discussed.
Quand le patient est atteint de brûlures de grande extension, pour les fibroblastes il devient difficile de migrer de la périphérie du tissu sain pour coloniser la zone lésée. Même dans ces conditions la guérison a lieu, ce qui est attribué à la différenciation des fibrocytes en circulation qui entrent dans la plaie. Ce type normal de cellule a été identifié dans les fibroblastes chéloïdaux: il exprime des marqueurs des fibrocytes et sécrète des protéines de la matrice extracellulaire. Les épreuves in vitro sur la contraction du collagène révèlent que les fibrocytes contractent le gel de collagène avec une efficacité similaire à celle des fibroblastes normaux. Les Auteurs concluent avec une discussion sur la contribution des fibrocytes à la formation des fibroblastes chéloïdaux dans la phase finale de la guérison des brûlures.
ABSTRACT
Over production of collagen and its abnormal assembly is the hallmark of abnormal scars such as keloids, a condition which reflects fibrosis of the skin. Fibrotic conditions of organs such as liver, lungs and eyes are characterized by low levels of decorin, a member of the small leucine proteoglycan family, which is an indispensable modulator of collagen assembly. Involvement of decorin in keloids is not well described, therefore, its expression in keloids was studied here. We showed low decorin levels in the total tissue extract of keloids as compared to normal skin. Further, we showed that this low level is due to reduced transcription of decorin by keloid fibroblasts. As decorin can also act as an intermediate signaling molecule involved in the ERK1,2 pathway, levels of both ERK1,2 and its activated counterpart were studied and found to be up-regulated in keloids. Through this study a novel attempt has been made to understand the implications of decorin expression and a possible cause of over production of collagen and its aberrant assembly in keloids is suggested.
