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不同血清对瘢痕疙瘩和正常皮肤成纤维细胞生长动力学及胶原蛋白合成的影响。

Effects of various sera on growth kinetics and collagen synthesis by keloid and normal dermal fibroblasts.

作者信息

McCoy B J, Cohen I K

出版信息

Plast Reconstr Surg. 1981 Apr;67(4):505-10. doi: 10.1097/00006534-198104000-00014.

DOI:10.1097/00006534-198104000-00014
PMID:7208694
Abstract

Fibroblasts derived from normal dermis and keloids were cultured in nutrient medium supplemented with fetal bovine serum, serum from keloid patients, and serum from age-, sex-, and race-matched nonkeloid formers. Cell numbers were determined at various times during the growth period, and collagen synthesis was analyzed on day 7. In lag phase, keloid-derived fibroblasts were significantly reduced in all sera compared with normal dermal fibroblasts. However, beyond day 2, the growth kinetics of both cell types were similar in keloid and control human sera. Furthermore, collagen synthesis relative to total protein synthesis (percent) was similar in keloid and control human sera. Although systemic factors have been implicated in the pathogenesis of keloids and other fibrotic diseases such as scleroderma and pulmonary fibrosis, this study demonstrates that serum from keloid patients does not contain a factor(s) that significantly modifies the in vitro growth kinetics or collagen synthesis of keloid-derived or normal dermal fibroblasts.

摘要

从正常真皮和瘢痕疙瘩中提取的成纤维细胞在补充有胎牛血清、瘢痕疙瘩患者血清以及年龄、性别和种族匹配的非瘢痕疙瘩形成者血清的营养培养基中培养。在生长期间的不同时间测定细胞数量,并在第7天分析胶原蛋白合成情况。在延迟期,与正常真皮成纤维细胞相比,在所有血清中瘢痕疙瘩来源的成纤维细胞显著减少。然而,在第2天之后,瘢痕疙瘩和对照人血清中两种细胞类型的生长动力学相似。此外,瘢痕疙瘩和对照人血清中相对于总蛋白合成的胶原蛋白合成(百分比)相似。虽然全身因素被认为与瘢痕疙瘩以及其他纤维化疾病(如硬皮病和肺纤维化)的发病机制有关,但本研究表明,瘢痕疙瘩患者的血清中不含有能显著改变瘢痕疙瘩来源或正常真皮成纤维细胞体外生长动力学或胶原蛋白合成的因子。

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引用本文的文献

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Effects of density and cellular aging on collagen synthesis and growth kinetics in keloid and normal skin fibroblasts.密度和细胞衰老对瘢痕疙瘩及正常皮肤成纤维细胞中胶原蛋白合成和生长动力学的影响。
In Vitro. 1982 Jan;18(1):79-86. doi: 10.1007/BF02796388.
2
Mitogenic effects of sera from normal and psoriatic subjects on human skin fibroblasts.
Arch Dermatol Res. 1985;277(1):13-5. doi: 10.1007/BF00406474.