The Effect of Myofibroblast on Contracture of Hypertrophic Scar

Abstract

Wound contraction in humans has both positive and negative effects. It is beneficial to wound healing by narrowing the wound margins, but the formation of undesirable scar contracture brings cosmetic and even functional problems. The entire mechanism of wound healing and scar contracture is not clear yet, but it is at least considered that both the fibroblasts and the myofibroblasts are responsible for contraction in healing wounds. The myofibroblast is a cell that possesses all the morphologic and biochemical characteristics of both a fibroblast and a smooth muscle cell. Normally, the myofibroblasts appear in the initial wound healing processes and generate contractile forces to pull both edges of an open wound until it disappears by apoptosis. But as an altered regulation of myofibroblast disappearance, they remain in the dermis and continuously contract the scar, eventually causing scar contracture. In this research, to compare and directly evaluate the influence on scar contracture of the myofibroblast versus the fibroblast, dermal tissues were taken from 10 patients who had highly contracted hypertrophic scars. The myofibroblasts were isolated and concentrated from the fibroblasts using the magnetic activating cell-sorting column to obtain the myofibroblast group, which contained about 28 to 41 percent of the myofibroblasts, and the fibroblast group, which contained less than 0.9 percent of the myofibroblasts. Each group was cultured in the fibroblast-populated collagen lattice for 13 days, and the contraction of the collagen gel was measured every other day. In addition, they were selectively treated with tranilast [N-(3',4'-dimethoxycinnamoyl) anthranilic acid] to evaluate the influence on the contraction of the collagen gel lattice. During the culture, the myofibroblast group, compared with the fibroblast group, showed statistically significant contraction of the collagen gel lattice day by day, except on the first day, and only the myofibroblast group was affected by tranilast treatment, showing significant inhibition of gel contraction. By utilizing an in vitro model, the authors have demonstrated that myofibroblasts play a more important role in the contracture of the hypertrophic scar.

Notch1 Signaling Regulates Wound Healing via Changing the Characteristics of Epidermal Stem Cells

“…α-SMA (a myofibroblast marker) and extracellular matrix (ECM) components, such as collagen I and collagen Ⅲ, are factors that are closely related to scar formation and contraction [28,29]. Similar to muscle cell contraction, myofibroblast contraction is dependent on α-SMA.…”

Wound-healing and potential anti-keloidal properties of the latex of <i>Calotropis procera</i> (aiton) asclepiadaceae in rabbits

“…Hypertrophic scars and keloids are aberrant forms of wound healing and are indications of exaggerated function of fibroblasts and excess accumulation of ECM during wound healing [Wen-Hsiang et al,2010] in which case there is a dysregulated response to cutaneous injuries, which results in an excessive deposition of collagen [Shin et al,2004]. Hypertrophic scars and keloids are not exactly same.…”

Growth factor pathways in hypertrophic scars: Molecular pathogenesis and therapeutic implications

“…Fibroblasts and myofibroblasts are able to generate contractile forces bringing together the edges of an open wound, which is responsible for wound contraction and closure during hypertrophic scars [14]. The contractile nature of myofibroblasts influences wound size and healing time, and leads to increased stiffness.…”