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人脂肪来源的干细胞抑制瘢痕疙瘩成纤维细胞的活性。

Human adipose-derived stem cells inhibit bioactivity of keloid fibroblasts.

机构信息

Department of Plastic and Reconstructive Surgery, Shanghai 9th People's Hospital, Shanghai Jiao Tong University School of Medicine, 639 Zhi Zao Ju Road, Shanghai, 200011, China.

Division of Plastic Surgery, Xinjiang Korla Bazhou People's Hospital, Xinjiang, China.

出版信息

Stem Cell Res Ther. 2018 Feb 21;9(1):40. doi: 10.1186/s13287-018-0786-4.

DOI:10.1186/s13287-018-0786-4
PMID:29467010
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC5822616/
Abstract

BACKGROUND

A keloid is a fibroproliferative disorder occurring in wounds characterized by an exaggerated response to injury. To date, no effective cure has been identified. As multipotent stem cells, human adipose-derived stem cells (ADSCs) may show the possibility for curing diseases such as fibrosis. This study sought to explore the potential role of human ADSCs in curing keloids.

METHODS

After culture in conditioned medium, gene and protein expression of keloid fibroblasts was examined using real-time polymerase chain reaction (RT-PCR) and Western blotting, while analysis of the cell cycle was used to measure the proliferative properties of the cells. Furthermore, ex vivo explant cultures were used to test the effects of ADSC-conditioned medium (ADSC-CM) on CD31 and CD34 expression in keloid tissue.

RESULTS

Our experimental results show that ADSC-CM was able to attenuate extracellular matrix-related gene expression as well as decrease protein expression. Cell proliferation was significantly suppressed in our study. CD31 and CD34 vessels in ex vivo explants were reduced by 55% and 57% in treatment groups compared with control groups.

CONCLUSIONS

Human ADSC-CM significantly inhibited keloid fibroblast-related bioactivities.

摘要

背景

瘢痕疙瘩是一种纤维增生性疾病,发生于创伤部位,表现为对损伤的过度反应。迄今为止,尚无有效的治疗方法。作为多能干细胞,人脂肪来源干细胞(ADSCs)可能显示出治疗纤维化等疾病的可能性。本研究旨在探讨人 ADSCs 在治疗瘢痕疙瘩中的潜在作用。

方法

在条件培养基中培养后,使用实时聚合酶链反应(RT-PCR)和 Western blot 检测瘢痕疙瘩成纤维细胞的基因和蛋白表达,同时分析细胞周期以测量细胞的增殖特性。此外,还进行了离体组织培养实验,以测试 ADSC 条件培养基(ADSC-CM)对瘢痕疙瘩组织中 CD31 和 CD34 表达的影响。

结果

我们的实验结果表明,ADSC-CM 能够减弱细胞外基质相关基因的表达,并降低蛋白表达。细胞增殖在我们的研究中受到显著抑制。与对照组相比,实验组离体组织中的 CD31 和 CD34 血管分别减少了 55%和 57%。

结论

人 ADSC-CM 可显著抑制瘢痕疙瘩成纤维细胞的相关生物活性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/99ef/5822616/752aa6d7a522/13287_2018_786_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/99ef/5822616/e5799654f24d/13287_2018_786_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/99ef/5822616/8eb003966600/13287_2018_786_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/99ef/5822616/5831715d4479/13287_2018_786_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/99ef/5822616/74e8064a999c/13287_2018_786_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/99ef/5822616/08a69a4c5daf/13287_2018_786_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/99ef/5822616/b5e8792470b5/13287_2018_786_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/99ef/5822616/752aa6d7a522/13287_2018_786_Fig7_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/99ef/5822616/e5799654f24d/13287_2018_786_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/99ef/5822616/8eb003966600/13287_2018_786_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/99ef/5822616/5831715d4479/13287_2018_786_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/99ef/5822616/74e8064a999c/13287_2018_786_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/99ef/5822616/08a69a4c5daf/13287_2018_786_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/99ef/5822616/b5e8792470b5/13287_2018_786_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/99ef/5822616/752aa6d7a522/13287_2018_786_Fig7_HTML.jpg

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