Suppressive effects of human fetal keratinocytes on the proliferation, differentiation and extracellular matrix synthesis of human hypertrophic scar fibroblasts in vitro.

Suppressive effects of human fetal keratinocytes on the proliferation, differentiation and extracellular matrix synthesis of human hypertrophic scar fibroblasts in vitro.
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DOI:
10.3892/mmr.2017.7220
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发表时间:
2017-10
影响因子:
3.4
通讯作者:
Li H
Li H
中科院分区:
医学4区
文献类型:
--
作者:
Wang Z;Song Q;Li H

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增生性瘢痕的特征在于成纤维细胞增殖和过量的细胞外基质沉积。新出现的证据表明,胎儿角质形成细胞(KCs)有助于无瘢痕伤口愈合。然而,胎儿角质形成细胞和增生性瘢痕之间的关系仍不清楚。在本研究中,分离不同胎龄的人KCs,并与人增生性瘢痕成纤维细胞(HSFbs)或正常皮肤成纤维细胞共培养。采用逆转录-定量聚合酶链反应(RT-PCR)和蛋白质印迹法(Western blot)检测成纤维细胞中纤维连接蛋白(FN)、胶原1(collagen 1)和α-平滑肌肌动蛋白(α-smooth muscle actin)的基因表达和蛋白水平。胎鼠KCs对体外培养的HSFbs增殖有明显的抑制作用。胎儿角质形成细胞还影响HSFbs中纤维连接蛋白、胶原1和α-平滑肌肌动蛋白的表达。此外,miR-940可能通过直接靶向转化生长因子-β1调节胎儿KCs对HSFbs细胞增殖、分化和细胞外基质合成的抑制作用。综上所述,本研究的结果提供了证据,以支持胎儿KCs的细胞为基础的治疗性移植在预防增生性瘢痕的潜在用途。
A hypertrophic scar is characterized by fibroblast proliferation and excessive extracellular matrix deposition. Emerging evidence has revealed that fetal keratinocytes (KCs) contribute to scarless wound healing. However, the association between fetal keratinocytes and hypertrophic scarring remains unclear. In the present study, human KCs of different gestational ages were isolated and co-cultured with human hypertrophic scar fibroblasts (HSFbs) or normal skin fibroblasts. Gene expression and protein levels of fibronectin, collagen 1and α-smooth muscle actin in the fibroblasts were measured by reverse transcription-quantitative polymerase chain reaction and western blot analyses. It was observed that fetal KCs significantly inhibited the proliferation of HSFbs in vitro. Fetal keratinocytes also affected the expression of fibronectin, collagen 1 and α-smooth muscle actin in HSFbs. In addition, miR-940 may modulate the suppressive effects of fetal KCs on the cell proliferation, differentiation and extracellular matrix synthesis of HSFbs by directly targeting transforming growth factor-β1. Taken together, the results of the present study provide evidence to support the potential use of fetal KCs for cell-based therapeutic grafting in the prevention of hypertrophic scarring.
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