Mikulec A A, Hanasono M M, Lum J, Kadleck J M, Kita M, Koch R J
Division of Otolaryngology/Head and Neck Surgery, Stanford University Medical Center, 300 Pasteur Dr, Stanford, CA 94305-5328, USA.
Arch Facial Plast Surg. 2001 Apr-Jun;3(2):111-4. doi: 10.1001/archfaci.3.2.111.
Evidence suggests that keloid scar formation may be mediated, in part, by deranged growth factor activity, including that of transforming growth factor (TGF) beta1. Tamoxifen citrate has shown promise in the treatment of keloids.
To evaluate the effect of tamoxifen on autocrine growth factor expression in keloid and fetal dermal fibroblasts, which exhibit scar-free healing.
Serum-free cell lines of keloid and fetal dermal fibroblasts were established. Cell cultures were exposed to different concentrations of tamoxifen solution (8 and 12 or 16 micromol/L). Cell counts were performed and supernatants collected at 24, 48, and 96 hours. Cell-free supernatants were quantitatively assayed for TGF-beta1 expression.
Keloid fibroblasts show increased per-cell TGF-beta1 production compared with fetal fibroblasts. Tamoxifen appeared to decrease per-cell TGF-beta1 production at each of the time points evaluated.
Keloids likely arise due to locally insufficient or excessive concentrations of specific growth factors. The higher level of TGF-beta1 produced by keloid cells compared with fetal fibroblasts could be related to the aberrant wound healing seen with keloids. The addition of tamoxifen may lead to improved wound healing in keloids by decreasing the expression of TGF-beta1.
有证据表明，瘢痕疙瘩的形成可能部分由生长因子活性紊乱介导，包括转化生长因子（TGF）β1的活性。枸橼酸他莫昔芬在瘢痕疙瘩的治疗中已显示出前景。
评估他莫昔芬对瘢痕疙瘩和胎儿真皮成纤维细胞自分泌生长因子表达的影响，胎儿真皮成纤维细胞表现为无瘢痕愈合。
建立瘢痕疙瘩和胎儿真皮成纤维细胞的无血清细胞系。细胞培养物暴露于不同浓度的他莫昔芬溶液（8和12或16 μmol/L）。在24、48和96小时进行细胞计数并收集上清液。对无细胞上清液进行TGF-β1表达的定量测定。
与胎儿成纤维细胞相比，瘢痕疙瘩成纤维细胞显示每细胞TGF-β1产生增加。在每个评估的时间点，他莫昔芬似乎都能降低每细胞TGF-β1的产生。
瘢痕疙瘩可能是由于局部特定生长因子浓度不足或过高引起的。与胎儿成纤维细胞相比，瘢痕疙瘩细胞产生的TGF-β1水平较高可能与瘢痕疙瘩中异常的伤口愈合有关。添加他莫昔芬可能通过降低TGF-β1的表达来改善瘢痕疙瘩的伤口愈合。
