瘢痕疙瘩中的成纤维细胞特性研究进展

王蕴璋; 苏晨; 付思祺; 刘立强

doi:10.3760/cma.j.cn501120-20210510-00176

瘢痕疙瘩中的成纤维细胞特性研究进展

doi: 10.3760/cma.j.cn501120-20210510-00176

1.
中国医学科学院整形外科医院整形九科，北京　　100144
2.
中山大学附属第八医院急诊科，深圳　　518033
3.
中南大学湘雅二医院皮肤科，长沙　　410011

详细信息

通讯作者:
刘立强，Email：liuliqiang@psh.pumc.edu.cn

计量
- 文章访问数: 304
- HTML全文浏览量: 56
- PDF下载量: 46
- 被引次数: 0
出版历程
- 收稿日期: 2021-05-10

Research advances on the characteristics of fibroblast in keloid

1.
Department Nine of Plastic Surgery,Plastic Surgery Hospital,Chinese Academy of Medical Sciences, Beijing 100144, China
2.
Emergency Department, the Eighth Affiliated Hospital of Sun Yat-sen University, Shenzhen 518033, China
3.
Department of Dermatology, the Second Xiangya Hospital, Central South University, Changsha 410011, China

More Information

Corresponding author: Liu Liqiang, Email: liuliqiang@psh.pumc.edu.cn

摘要

摘要: 近20年来，细胞生物学技术的发展推动了瘢痕疙瘩的相关研究。瘢痕疙瘩成纤维细胞（KFb）是瘢痕疙瘩中的主要效应细胞，与瘢痕疙瘩的发生发展密切相关。KFb在生物学特性、基因表达等方面与正常成纤维细胞有明显差异。该文从多个角度对KFb的特性进行了综述，详细描述了其生物学特性如显微结构、代谢特点、增殖性质等情况，并介绍了KFb的异质性与基因组学等方面的主要特征。对KFb研究的不断深入将有助于阐明瘢痕疙瘩的发病机制并为瘢痕疙瘩的防治提供宝贵策略。
- 瘢痕疙瘩 /
- 成纤维细胞 /
- 基因 /
- 生物学特性 /
- 信号通路
Abstract: In re-cent 20 years, the development of cell biology technology has promoted the research of keloid. Keloid fibroblasts (KFbs) are the main effector cells in keloid, which are closely related to the occurrence and development of keloid. It is significantly different in terms of biological characteristics and gene expression between KFbs and normal fibroblasts. This articles reviews the characteristics of KFbs from multiple perspectives, describing its biological character- istics in details including microstructures, metabolic character- istics, and proliferation properties, and introducing the main characteristics of heterogeneity and genomics of KFbs. The further research on KFbs will help to elucidate the pathogenesis of keloids and provide valuable strategies for the prevention and treatment of keloids.
- Keloid /
- Fibroblasts /
- Genes /
- Biological characteristics /
- Signaling pathway
所有作者均声明不存在利益冲突

HTML全文

表1 13篇文献的瘢痕疙瘩成纤维细胞微阵列芯片研究结果

第1作者	年份	类别	微阵列芯片分析
Hsu^［5］	2018	基因	345种基因↑，86种基因↓
Inui^［38］	2011	基因	374种基因↑，758种基因↓
Wong^［39］	2014	基因	250种基因差异表达
Satish^［40］	2006	基因	43种基因↑，5种基因↓
Seifert^［31］	2008	基因	97种基因↑，26种基因↓
Hahn^［41］	2013	基因	12种基因↑，13种基因↓
Li^［42］	2016	基因	196种基因↑，462种基因↓
郭晓瑞^［43］	2011	miR	1种miR↑，11种miR↓
Wu^［35］	2014	miR	3种miR↑，14种miR↓
Wu^［44］	2019	miR	63种miR↑，76种miR↓
Yan^［45］	2020	miR	14种miR↑，15种miR↓
Liang^［46］	2015	lncRNA	1 731种lncRNA↑，782种lncRNA↓
Guo^［47］	2016	lncRNA	1 290种lncRNA↑，778种lncRNA↓
注：miR为微小RNA, lncRNA为长链非编码RNA；↑表示上调，↓表示下调

下载: 导出CSV

《中华烧伤与创面修复杂志》第六届编辑委员会通讯编委名单按姓氏拼音排序

贲道锋	卞徽宁	曹永倩	晁生武	陈辉	陈婧	陈朗	陈铭锐	陈鹏	陈晓东
陈忠勇	程君涛	迟云飞	储国平	党永明	邓呈亮	狄海萍	丁国兵	丁若虹	董茂龙
段红杰	段鹏	樊东力	房贺	冯光	付忠华	郭毅斌	韩兆峰	侯春胜	胡德林
胡炯宇	胡骁骅	胡晓燕	黄红军	纪世召	江华	姜丽萍	姜玉峰	雷娜	黎宁
李东杰	李峰	李靖	李晓东	李晓鲁	梁钢	梁鹏飞	林才	林国安	林源
刘德伍	刘健	刘军	刘淑华	龙奕	卢长虹	鲁峰	吕开阳	吕强	马思远
牛轶雯	欧阳军	乔亮	覃凤均	邱学文	曲滨	任超	沈江涌	石继红	宋慧锋
苏海涛	苏永涛	孙勇	孙瑜	谭江琳	唐修俊	滕苗	田社民	涂家金	汪虹
汪洋	王爱萍	王德怀	王洪涛	王会军	王良喜	王爽	王献珍	王志永	温冰
邬佳敏	吴红	吴继炎	吴巍巍	吴祖煌	向飞	向军	谢举临	谢松涛	辛海明
许喜生	许学文	薛斌	杨建民	杨敏烈	杨薛康	姚明	姚兴伟	叶祥柏	易成刚
易南	于东宁	岳丽青	翟红军	詹日兴	张博	张东霞	张红艳	张菊芳	张玲娟
张庆红	张彦琦	张寅	张元海	张志	赵全	赵冉	赵雄	郑德义	郑东风
郑军	周国富	周俊峄	周琴	周万芳	朱峰	朱宇刚	祝筱梅	邹立津	邹晓防

下载: 导出CSV

参考文献(48)

[1]	OgawaR, AkitaS, AkaishiS, et al. Diagnosis and treatment of keloids and hypertrophic scars-Japan Scar Workshop Consensus Document 2018[J/OL]. Burns Trauma, 2019,7:39[2022-04-15]. https://pubmed.ncbi.nlm.nih.gov/31890718/. DOI: 10.1186/s41038-019-0175-y.
[2]	LuoL, LiJ, LiuH, et al. Adiponectin is involved in connective tissue growth factor-induced proliferation, migration and overproduction of the extracellular matrix in keloid fibroblasts[J]. Int J Mol Sci, 2017, 18(5):1044.DOI: 10.3390/ijms18051044.
[3]	FangF, HuangRL, ZhengY, et al. Bone marrow derived mesenchymal stem cells inhibit the proliferative and profibrotic phenotype of hypertrophic scar fibroblasts and keloid fibroblasts through paracrine signaling[J]. J Dermatol Sci, 2016,83(2):95-105. DOI: 10.1016/j.jdermsci.2016.03.003.
[4]	ZhangGY, GaoWY, LiX, et al. Effect of camptothecin on collagen synthesis in fibroblasts from patients with keloid[J]. Ann Plast Surg, 2009,63(1):94-99. DOI: 10.1097/SAP.0b013e3181872775.
[5]	HsuCK, LinHH, HarnHI, et al. Caveolin-1 controls hyperresponsiveness to mechanical stimuli and fibrogenesis- associated RUNX2 activation in keloid fibroblasts[J]. J Invest Dermatol, 2018,138(1):208-218. DOI: 10.1016/j.jid.2017.05.041.
[6]	AshcroftKJ, SyedF, BayatA. Site-specific keloid fibroblasts alter the behaviour of normal skin and normal scar fibroblasts through paracrine signalling[J]. PLoS One, 2013,8(12):e75600. DOI: 10.1371/journal.pone.0075600.
[7]	LimCP, PhanTT, LimIJ, et al. Cytokine profiling and Stat3 phosphorylation in epithelial-mesenchymal interactions between keloid keratinocytes and fibroblasts[J]. J Invest Dermatol, 2009,129(4):851-861. DOI: 10.1038/jid.2008.337.
[8]	VincentAS, PhanTT, MukhopadhyayA, et al. Human skin keloid fibroblasts display bioenergetics of cancer cells[J]. J Invest Dermatol, 2008,128(3):702-709. DOI: 10.1038/sj.jid.5701107.
[9]	LiQ, QinZ, NieF, et al. Metabolic reprogramming in keloid fibroblasts: aerobic glycolysis and a novel therapeutic strategy[J]. Biochem Biophys Res Commun, 2018,496(2):641-647. DOI: 10.1016/j.bbrc.2018.01.068.
[10]	苏治国, 范金财, 刘立强, 等. 瘢痕疙瘩成纤维细胞中Warburg效应的研究[J]. 中华整形外科杂志,2020,36(10):1100-1105. DOI: 10.3760/cma.j.cn114453-20200220-00064.
[11]	陈斌, 于东宁, 秦泽莲, 等. 瘢痕疙瘩成纤维细胞线粒体功能障碍及其对细胞代谢功能的影响[J].中华整形外科杂志, 2016, 32(5):359-64. DOI: 10.3760/cma.j.issn.1009-4598.2016.05.010.
[12]	XinY, WangX, ZhuM, et al. Expansion of CD26 positive fibroblast population promotes keloid progression[J]. Exp Cell Res, 2017,356(1):104-113. DOI: 10.1016/j.yexcr.2017.04.021.
[13]	LimandjajaGC, NiessenFB, ScheperRJ, et al. The keloid disorder: heterogeneity, histopathology, mechanisms and models[J]. Front Cell Dev Biol, 2020,8:360. DOI: 10.3389/fcell.2020.00360.
[14]	季江, 吴文雅, 经晶, 等. 瘢痕疙瘩成纤维细胞与正常人皮肤成纤维细胞增殖和胶原产生及相关基因的表达[J]. 中华医学美学美容杂志, 2015, 21(6):361-364. DOI: 10.3760/cma.j.issn.1671-0290.2015.06.013.
[15]	DengCC, ZhuDH, ChenYJ, et al. TRAF4 promotes fibroblast proliferation in keloids by destabilizing p53 via interacting with the deubiquitinase USP10[J]. J Invest Dermatol, 2019,139(9):1925-1935.e5. DOI: 10.1016/j.jid.2019.03.1136.
[16]	YuD, ShangY, YuanJ, et al. Wnt/β-catenin signaling exacerbates keloid cell proliferation by regulating telomerase[J]. Cell Physiol Biochem, 2016,39(5):2001-2013. DOI: 10.1159/000447896.
[17]	HoffmeyerK, RaggioliA, RudloffS, et al. Wnt/β-catenin signaling regulates telomerase in stem cells and cancer cells[J]. Science, 2012,336(6088):1549-1554. DOI: 10.1126/science.1218370.
[18]	LiY, LiuH, LiangY, et al. DKK3 regulates cell proliferation, apoptosis and collagen synthesis in keloid fibroblasts via TGF-β1/Smad signaling pathway[J]. Biomed Pharmacother, 2017,91:174-180. DOI: 10.1016/j.biopha.2017.03.044.
[19]	郭洪耀, 乔军波, 林斌, 等. DKK3基因过表达对人瘢痕疙瘩成纤维细胞增殖和凋亡的影响 [J]. 郑州大学学报(医学版), 2019, 54(3): 474-477. DOI: 10.13705/j.issn.1671-6825.2018.09.120.
[20]	姚晓东MiR-1224-5p通过TGF-β₁苏州苏州大学2018 姚晓东. MiR-1224-5p通过TGF-β1/Smad3通路影响瘢痕疙瘩成纤维细胞增殖、凋亡及侵袭 [D].苏州:苏州大学, 2018.
[21]	WuH, WangJ, MaH, et al. MicroRNA-21 inhibits mitochondria-mediated apoptosis in keloid[J]. Oncotarget, 2017,8(54):92914-92925. DOI: 10.18632/oncotarget.21656.
[22]	ZhaoX, JieX, GaoYK, et al. Long non-coding RNA CACNA1G-AS1 promotes proliferation and invasion and inhibits apoptosis by regulating expression of miR-205 in human keloid fibroblasts[J]. Biosci Rep, 2020,40(6):BSR20192839.DOI: 10.1042/BSR20192839.
[23]	WangZ, FengC, SongK, et al. lncRNA-H19/miR-29a axis affected the viability and apoptosis of keloid fibroblasts through acting upon COL1A1 signaling[J]. J Cell Biochem, 2020,121(11):4364-4376. DOI: 10.1002/jcb.29649.
[24]	XuL, SunN, LiG, et al. LncRNA H19 promotes keloid formation through targeting the miR-769-5p/EIF3A pathway[J]. Mol Cell Biochem, 2021,476(3):1477-1487. DOI: 10.1007/s11010-020-04024-x.
[25]	陆长玺, 郭传瑸. 成釉细胞瘤基质金属蛋白酶-2表达的初步研究[J]. 口腔颌面外科杂志, 2021, 31(1): 28-31. DOI: 10.3969/j.issn.1005-4979.2021.01.005.
[26]	张鹏, 纪亮, 张翠香,等. 基质金属蛋白酶促进瘢痕疙瘩成纤维细胞迁移及其意义[J]. 中国现代医学杂志, 2013, 23(3): 11-14.
[27]	徐志山, 回蔷, 李伟, 等. miR-194-3p对瘢痕疙瘩成纤维细胞迁移的作用 [J]. 中华整形外科杂志, 2018, 34(11): 964-970. DOI: 10.3760/cma.j.issn.1009-4598.2018.11.018.
[28]	田怡肿瘤侵犯相关蛋白AMF对人瘢痕疙瘩成纤维细胞增殖迁移作用的影响及机制研究重庆重庆医科大学2016 田怡. 肿瘤侵犯相关蛋白AMF对人瘢痕疙瘩成纤维细胞增殖迁移作用的影响及机制研究 [D].重庆:重庆医科大学, 2016.
[29]	desJardins-ParkHE, ChintaMS, FosterDS, et al. Fibroblast heterogeneity in and its implications for plastic and reconstructive surgery: a basic science review[J]. Plast Reconstr Surg Glob Open, 2020,8(6):e2927. DOI: 10.1097/GOX.0000000000002927.
[30]	XinY, MinP, XuH, et al. CD26 upregulates proliferation and invasion in keloid fibroblasts through an IGF-1-induced PI3K/AKT/mTOR pathway[J/OL]. Burns Trauma, 2020,8:tkaa025[2022-03-16]. https://pubmed.ncbi.nlm.nih.gov/33150188/.DOI: 10.1093/burnst/tkaa025.
[31]	SeifertO, BayatA, GeffersR, et al. Identification of unique gene expression patterns within different lesional sites of keloids[J]. Wound Repair Regen, 2008,16(2):254-265. DOI: 10.1111/j.1524-475X.2007.00343.x.
[32]	LuF, GaoJ, OgawaR, et al. Biological differences between fibroblasts derived from peripheral and central areas of keloid tissues[J]. Plast Reconstr Surg, 2007,120(3):625-630. DOI: 10.1097/01.prs.0000270293.93612.7b.
[33]	Tucci-ViegasVM, HochmanB, FrançaJP, et al. Keloid explant culture: a model for keloid fibroblasts isolation and cultivation based on the biological differences of its specific regions[J]. Int Wound J, 2010,7(5):339-348. DOI: 10.1111/j.1742-481X.2010.00698.x.
[34]	SyedF, AhmadiE, IqbalSA, et al. Fibroblasts from the growing margin of keloid scars produce higher levels of collagen I and Ⅲ compared with intralesional and extralesional sites: clinical implications for lesional site-directed therapy[J]. Br J Dermatol, 2011,164(1):83-96. DOI: 10.1111/j.1365-2133.2010.10048.x.
[35]	WuZY, LuL, LiangJ, et al. Keloid microRNA expression analysis and the influence of miR-199a-5p on the proliferation of keloid fibroblasts[J]. Genet Mol Res, 2014,13(2):2727-2738. DOI: 10.4238/2014.April.14.2.
[36]	XuZ, GuoB, ChangP, et al. The differential expression of miRNAs and a preliminary study on the mechanism of miR-194-3p in keloids[J]. Biomed Res Int, 2019,2019:8214923. DOI: 10.1155/2019/8214923.
[37]	ZhangQ, YamazaT, KellyAP, et al. Tumor-like stem cells derived from human keloid are governed by the inflammatory niche driven by IL-17/IL-6 axis[J]. PLoS One, 2009,4(11):e7798. DOI: 10.1371/journal.pone.0007798.
[38]	InuiS, ShonoF, NakajimaT, et al. Identification and characterization of cartilage oligomeric matrix protein as a novel pathogenic factor in keloids[J]. Am J Pathol, 2011,179(4):1951-1960. DOI: 10.1016/j.ajpath.2011.06.034.
[39]	WongVW, YouF, JanuszykM, et al. Transcriptional profiling of rapamycin-treated fibroblasts from hypertrophic and keloid scars[J]. Ann Plast Surg, 2014,72(6):711-719. DOI: 10.1097/SAP.0b013e31826956f6.
[40]	SatishL, Lyons-WeilerJ, HebdaPA, et al. Gene expression patterns in isolated keloid fibroblasts[J]. Wound Repair Regen, 2006,14(4):463-470. DOI: 10.1111/j.1743-6109.2006.00135.x.
[41]	HahnJM, GlaserK, McFarlandKL, et al. Keloid-derived keratinocytes exhibit an abnormal gene expression profile consistent with a distinct causal role in keloid pathology[J]. Wound Repair Regen, 2013,21(4):530-544. DOI: 10.1111/wrr.12060.
[42]	LiM, WuL. Functional analysis of keratinocyte and fibroblast gene expression in skin and keloid scar tissue based on deviation analysis of dynamic capabilities[J]. Exp Ther Med, 2016,12(6):3633-3641. DOI: 10.3892/etm.2016.3817.
[43]	郭晓瑞MicroRNAs在瘢痕疙瘩中差异表达的研究广州广东医学院2011DOI: 10.7666/d.y2013019 郭晓瑞. MicroRNAs在瘢痕疙瘩中差异表达的研究[D]. 广州:广东医学院,2011. DOI: 10.7666/d.y2013019.
[44]	WuJ, FangL, CenY, et al. MiR-21 regulates keloid formation by downregulating Smad7 via the TGF-β/Smad signaling pathway[J]. J Burn Care Res, 2019,40(6):809-817. DOI: 10.1093/jbcr/irz089.
[45]	YanL, WangLZ, XiaoR, et al. Inhibition of microRNA-21-5p reduces keloid fibroblast autophagy and migration by targeting PTEN after electron beam irradiation[J]. Lab Invest, 2020,100(3):387-399. DOI: 10.1038/s41374-019-0323-9.
[46]	LiangX, MaL, LongX, et al. LncRNA expression profiles and validation in keloid and normal skin tissue[J]. Int J Oncol, 2015,47(5):1829-1838. DOI: 10.3892/ijo.2015.3177.
[47]	GuoL, XuK, YanH, et al. Expression profile of long noncoding RNAs in human earlobe keloids: a microarray analysis[J]. Biomed Res Int, 2016,2016:5893481. DOI: 10.1155/2016/5893481.
[48]	Ud-DinS, BayatA. Keloid scarring or disease: unresolved quasi-neoplastic tendencies in the human skin[J]. Wound Repair Regen, 2020,28(3):422-426. DOI: 10.1111/wrr.12793.