神经再生相关蛋白在皮肤纤维化中的作用机制研究进展

陈伟; 徐广超; 黄仲路; 陈丽; 聂开瑜

doi:10.3760/cma.j.cn501225-20220701-00278

神经再生相关蛋白在皮肤纤维化中的作用机制研究进展

doi: 10.3760/cma.j.cn501225-20220701-00278

遵义医科大学附属医院烧伤整形外科，遵义　　563003

基金项目:

省部共建协同创新中心项目 2020-39

详细信息

通讯作者:
聂开瑜，Email：1147900529@qq.com

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- 被引次数: 0
出版历程
- 收稿日期: 2022-07-01

Research advances on the mechanism of nerve regeneration-related protein in skin fibrosis

Department of Burns and Plastic Surgery, Affiliated Hospital of Zunyi Medical University, Zunyi 563003, China

Funds:

Collaborative Innovation Center of Chinese Ministry of Education 2020-39

More Information

Corresponding author: Nie Kaiyu, Email: 1147900529@qq.com

摘要

摘要: 皮肤损伤后的愈合是多种细胞、细胞因子及细胞外基质相互作用的动态过程，纤维化是皮肤损伤修复的主要方式之一。纤维化过程涉及多种因素调节，研究显示神经再生相关蛋白（NREP）在皮肤组织和脏器的纤维化中起关键作用。该文从皮肤纤维化的机制出发，探讨NREP三级结构的构建，归纳NREP与皮肤中不同细胞对皮肤纤维化的影响、NREP在皮肤纤维化中的作用机制研究进展，以为皮肤纤维化疾病的治疗提供新的思路。
- 皮肤 /
- 瘢痕 /
- 纤维化 /
- 神经再生相关蛋白
Abstract: The healing process after skin injury is a dynamic process of interaction between various cells, cytokines, and extracellular matrix. Fibrosis is one of the main ways of skin injury repair. The process of fibrosis involves the regulation of many factors. Studies have shown that nerve regeneration-related protein (NREP) plays a key role in the fibrosis of skin tissue and organs. Based on the mechanism of skin fibrosis, this paper discusses the construction of tertiary structure of NREP, summarizes the effects of NREP and different cells in the skin on skin fibrosis and the research progress of mechanism of NREP in skin fibrosis, thus providing new ideas for the treatment of skin fibrosis diseases.
- Skin /
- Cicatrix /
- Fibrosis /
- Nerve regeneration-related protein
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参考文献(41)

[1]	StudlerJM,GlowinskiJ,Lévi-StraussM.An abundant mRNA of the embryonic brain persists at a high level in cerebellum, hippocampus and olfactory bulb during adulthood[J].Eur J Neurosci,1993,5(6):614-623.DOI: 10.1111/j.1460-9568.1993.tb00527.x.
[2]	StradiotL, MannaertsI, van GrunsvenLA. P311, friend, or foe of tissue fibrosis?[J]. Front Pharmacol,2018,9: 1151.DOI: 10.3389/fphar.2018.01151.
[3]	PengX,YuanSZ,TanJL,et al. Identification of ITGB4BP as a new interaction protein of P311[J].Life Sci,2012,90(15/16):585-590.DOI: 10.1016/j.lfs.2012.02.008.
[4]	LiuY,ZhouXH,HuNY,et al.P311 regulates distal lung development via its interaction with several binding proteins[J].Mech Dev,2020,163:103633.DOI: 10.1016/j.mod.2020.103633.
[5]	MarianiL,McDonoughWS,HoelzingerDB,et al.Identification and validation of P311 as a glioblastoma invasion gene using laser capture microdissection[J].Cancer Res,2001,61(10):4190-4196.
[6]	KimH, KimJH, KimSY, et al. Meta-analysis of large-scale toxicogenomic data finds neuronal regeneration related protein and cathepsin D to be novel biomarkers of drug-induced toxicity[J]. PLoS One,2016, 11(9): e0163403.DOI: 10.1371/journal.pone.0163403.
[7]	ChengT,YueM,AslamMN,et al. Neuronal protein 3.1 deficiency leads to reduced cutaneous scar collagen deposition and tensile strength due to impaired transforming growth factor-β1 to -β3 translation[J]. Am J Pathol, 2017,187(2):292-303.DOI: 10.1016/j.ajpath.2016.10.004.
[8]	DuanFF,BarronG, MelitonA, et al. P311 promotes lung fibrosis via stimulation of transforming growth factor-β1, -β2, and -β3 tanslation[J]. Am J Respir Cell Mol Biol,2019,60(2): 221-231.DOI: 10.1165/rcmb.2018-0028OC.
[9]	PaliwalS,ShiJH,DhruU,et al.P311 binds to the latency associated protein and downregulates the expression of TGF-β1 and TGF-β2[J].Biochem Biophys Res Commun,2004,315(4):1104-1109.DOI: 10.1016/j.bbrc.2004.01.171.
[10]	YaoZH, LiHS, HeWF, et al. P311 accelerates skin wound reepithelialization by promoting epidermal stem cell migration through RhoA and Rac1 activation[J]. Stem Cells Dev,2017, 26(6): 451-460.DOI: 10.1089/scd.2016.0249.
[11]	TanJL,PengX,LuoGX,et al.Investigating the role of P311 in the hypertrophic scar[J].PLoS One,2010,5(4):e9995.DOI: 10.1371/journal.pone.0009995.
[12]	ThulabanduV,ChenD,AtitRP.Dermal fibroblast in cutaneous development and healing[J].Wiley Interdiscip Rev Dev Biol,2018,7(2): 10.1002/wdev.307.DOI: 10.1002/wdev.307.
[13]	HongYK, ChangYH, LinYC, et al. Inflammation in wound healing and pathological scarring[J]. Adv Wound Care (New Rochelle),2023, 12(5): 288-300.DOI: 10.1089/wound.2021.0161.
[14]	KarppinenSM,HeljasvaaraR,GullbergD,et al.Toward understanding scarless skin wound healing and pathological scarring[J].F1000Res,2019,8: F1000 Faculty Rev-787.DOI: 10.12688/f1000research.18293.1.
[15]	WangZC, ZhaoWY, CaoYY, et al. The roles of inflammation in keloid and hypertrophic scars[J]. Front Immunol,2020, 11: 603187.DOI: 10.3389/fimmu.2020.603187.
[16]	ElAttarY,MouradB,AlngomyHA,et al.Study of interleukin-1 beta expression in acne vulgaris and acne scars[J].J Cosmet Dermatol,2022,21(10):4864-4870.DOI: 10.1111/jocd.14852.
[17]	DengCC,HuYF,ZhuDH,et al.Single-cell RNA-seq reveals fibroblast heterogeneity and increased mesenchymal fibroblasts in human fibrotic skin diseases[J].Nat Commun,2021,12(1):3709.DOI: 10.1038/s41467-021-24110-y.
[18]	KakinumaT,KagimotoM,KanekoA,et al.Prevention and management of hypertrophic scars after laparoscopic surgery using silicone gel sheets: a pilot study[J].J Int Med Res,2022,50(8):3000605221107597.DOI: 10.1177/03000605221107597.
[19]	FrangogiannisN.Transforming growth factor-β in tissue fibrosis[J].J Exp Med,2020,217(3):e20190103.DOI: 10.1084/jem.20190103.
[20]	MascharakS,desJardins-ParkHE,DavittMF,et al.Preventing Engrailed-1 activation in fibroblasts yields wound regeneration without scarring[J].Science,2021,372(6540):eaba2374.DOI: 10.1126/science.aba2374.
[21]	BrewerCM,NelsonBR,WakenightP,et al.Adaptations in Hippo-Yap signaling and myofibroblast fate underlie scar-free ear appendage wound healing in spiny mice[J].Dev Cell,2021,56(19):2722-2740.e6.DOI: 10.1016/j.devcel.2021.09.008.
[22]	WeiZY, HanC, LiHS, et al. Molecular mechanism of mesenchyme homeobox 1 in transforming growth factor β1-induced P311 gene transcription in fibrosis[J]. Front Mol Biosci,2020, 7: 59.DOI: 10.3389/fmolb.2020.00059.
[23]	薛晓怡,冯铁男,王群群,等.P311蛋白与金属硫蛋白ⅡA相互作用位点的计算机预测[J].上海大学学报(自然科学版),2011,17(6):728-733.DOI: 10.3969/j.issn.1007-2861.2011.06.008.
[24]	YueMM,LvKS,MeredithSC,et al.Novel RNA-binding protein P311 binds eukaryotic translation initiation factor 3 subunit b (eIF3b) to promote translation of transforming growth factor β1-3 (TGF-β1-3)[J].J Biol Chem,2014,289(49):33971-33983.DOI: 10.1074/jbc.M114.609495.
[25]	卫志远 TGF-β1调控成纤维细胞P311转录的机制研究重庆陆军军医大学 2020 卫志远.TGF-β1调控成纤维细胞P311转录的机制研究[D].重庆:陆军军医大学,2020.
[26]	袁顺宗,彭旭,马兵,等.利用免疫共沉淀验证HT036与P311间的相互作用[J].第三军医大学学报,2006,28(24):2400-2402.DOI: 10.3321/j.issn:1000-5404.2006.24.003.
[27]	周小海,刘宇,胡乃月,等.神经元蛋白3.1结合蛋白的筛选与鉴定[J].生物化学与生物物理进展,2010,37(12):1303-1312.DOI: 10.3724/SP.J.1206.2010.00283.
[28]	SuCT, UrbanZ. LTBP4 in health and disease[J]. Genes(Basel),2021, 12(6):795.DOI: 10.3390/genes12060795.
[29]	TanJL,LuoGX,WuJ.The biological roles of ITGB4BP and its potential effect on fibrosis[J].Int J Burns Trauma,2011,1(1):51-55.
[30]	MarconiGD, FonticoliL, RajanTS, et al. Epithelial-mesenchymal transition (EMT): the type-2 EMT in wound healing, tissue regeneration and organ fibrosis[J]. Cells,2021, 10(7): 1587.DOI: 10.3390/cells10071587.
[31]	JiangDS,ChristS,Correa-GallegosD,et al.Injury triggers fascia fibroblast collective cell migration to drive scar formation through N-cadherin[J].Nat Commun,2020,11(1):5653.DOI: 10.1038/s41467-020-19425-1.
[32]	SoundararajanM, KannanS. Fibroblasts and mesenchymal stem cells: two sides of the same coin?[J]. J Cell Physiol,2018, 233(12): 9099-9109.DOI: 10.1002/jcp.26860.
[33]	BuechlerMB,PradhanRN,KrishnamurtyAT,et al.Cross-tissue organization of the fibroblast lineage[J].Nature,2021,593(7860):575-579.DOI: 10.1038/s41586-021-03549-5.
[34]	PanD,ZheXN,JakkarajuS,et al.P311 induces a TGF-beta1-independent, nonfibrogenic myofibroblast phenotype[J].J Clin Invest,2002,110(9):1349-1358.DOI: 10.1172/JCI15614.
[35]	张路,李海胜,姚智慧,等.P311和转化生长因子β1相互作用及其对小鼠成纤维细胞功能的影响[J].中华烧伤杂志,2016,32(4):208-215.DOI: 10.3760/cma.j.issn.1009-2587.2016.04.005.
[36]	LiuJQ,ZhaoB,ZhuHY,et al.Wnt4 negatively regulates the TGF-β1-induced human dermal fibroblast-to-myofibroblast transition via targeting Smad3 and ERK[J].Cell Tissue Res,2020,379(3):537-548.DOI: 10.1007/s00441-019-03110-x.
[37]	NunezS,YoungC,AdebayoO,et al.P311, a novel intrinsically disordered protein, regulates adipocyte development[J].Biochem Biophys Res Commun,2019,515(1):234-240.DOI: 10.1016/j.bbrc.2019.05.105.
[38]	LiHS,YaoZH,HeWF,et al.P311 induces the transdifferentiation of epidermal stem cells to myofibroblast-like cells by stimulating transforming growth factor β1 expression[J].Stem Cell Res Ther,2016,7(1):175.DOI: 10.1186/s13287-016-0421-1.
[39]	ZhouDJ,LiuTF, WangS, et al. Effects of IL-1β and TNF-α on the expression of P311 in vascular endothelial cells and wound healing in mice[J]. Front Physiol,2020, 11: 545008.DOI: 10.3389/fphys.2020.545008.
[40]	WangS, ZhangXR, QianW, et al. P311 deficiency leads to attenuated angiogenesis in cutaneous wound healing[J]. Front Physiol,2017, 8: 1004.DOI: 10.3389/fphys.2017.01004.
[41]	XuM, XuHH, LinY, et al. LECT2, a ligand for Tie1, plays a crucial role in liver fibrogenesis[J]. Cell,2019, 178(6): 1478-1492.e20.DOI: 10.1016/j.cell.2019.07.021.