Akihiro Aioi
Septem Soken Co., Ltd. 、School of Med, University of Queensland
Pei-Yun Liu, Roy Kimble, James McMillan
School of Med, University of Queensland

[Abstract]
Hypertrophic scarring and keloid are disfiguring and functionally limiting dermal connective tissue proliferation in slow-to-heal burn wounds. Myofibroblasts differentiated from fibroblasts with α-SMA expression play important roles in wound closure with a complex cytokine network. However, the precise network of control mechanisms and complete range of cytokines involved that lead to the formation and persistence of myofibroblasts in hypertrophic scarring and keloid remains to be fully investigated. We present here the role of IL-6 on α-SMA expression in some types of fibroblasts. The ratio of α-SMA positive cell in fibroblasts derived from hypertrophic scarring (HSF) increased significantly, compared with normal human dermal fibroblasts (NHDF). Likewise the expression of α-SMA in fibroblasts treated with TGF-β1 (NHDF+T) was significantly enhanced, concomitant with IL-6 and collagen expression. To explore the role of IL-6 on α-SMA expression, we added IL-6 alone to culture media and performed neutralization experiments with anti IL-6 mAb. IL-6 induced significantly α-SMA expression, but the ratio was much weaker than in NHDF+T. In neutralization experiments, anti IL-6 mAb did not affect the expression of α-SMA induced by TGF-β1. On the other hand, α-SMA expression was observed in fibroblasts derived from keloid (KF), but the shape of cells was different from HSF and NHDF+T. The production of IL-6 from KF is equivalent to or less than NHDF. Taken together, these results suggest that IL-6 involves in α-SMA expression, but its role is not critical in NHDF+T. It is supposed that other signal cascade to induce α-SMA expression exists in KF, not depending on IL-6.