Volume 38 Issue 6
Jun.  2022
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Wang YZ,Su C,Fu SQ,et al.Research advances on the characteristics of fibroblast in keloid[J].Chin J Burns Wounds,2022,38(6):590-594.DOI: 10.3760/cma.j.cn501120-20210510-00176.
Citation: Wang YZ,Su C,Fu SQ,et al.Research advances on the characteristics of fibroblast in keloid[J].Chin J Burns Wounds,2022,38(6):590-594.DOI: 10.3760/cma.j.cn501120-20210510-00176.

Research advances on the characteristics of fibroblast in keloid

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

     

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  • [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.
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