中华整形外科杂志
中華整形外科雜誌
중화정형외과잡지
CHINESE JOURNAL OF PLASTIC SURGERY
2011年
6期
453-460
,共8页
计算生物学%瘢痕,肥大性%皮肤
計算生物學%瘢痕,肥大性%皮膚
계산생물학%반흔,비대성%피부
Computational biology%Cicatrix,hypertrophic%Skin
目的 比较增生性瘢痕(hypertrophic scar,HS)与正常皮肤的基因表达差异,从分子水平揭示HS的发病机制,为其临床防治提供新思路.方法 利用PubMed公共数据库文献挖掘HS与正常皮肤的差异表达基因,确定HS相关基因,并进行蛋白-蛋白相互作用网络、生物学通路、GeneOntology(基因本体)和功能注释聚类等生物信息学分析.结果 筛选HS相关基因55个(上调基因46个,下调基因9个).51个基因构成蛋白-蛋白相互作用网络,其中上调基因TGFB1、FN1、JUN、COL1A1、CTGF、VEGFA、FOS、COL3A1、IGF1、IL4、PELO、SMAD2、TIMP1、PCNA、ITGA4和下调基因ITGB1和DCN为此网络中心节点.HS相关基因参与黏着斑形成、整合素信号转导和肿瘤相关等生物学通路.并在细胞表面受体介导和胞内信号转导、组织发育与形态发生、细胞凋亡与增殖、大分子合成与代谢等生物过程,钙离子结合、双链DNA结合、启动子结合、肝素结合和促分裂素原活化蛋白激酶(MAPK)激活等分子功能中起着重要作用.功能注释聚类显示,HS相关基因多与表皮组织发育,血管生成,以及细胞凋亡调控有关.结论 TGFB1、FN1、JUN等关键基因,以及表皮组织发育,血管生成,以及细胞外基质-整合素-黏着斑相关的生物学通路、生物学过程和分子功能在HS的发生发展中可能起着重要作用,对其进一步分析有利于揭示HS的发病机制,并为临床治疗提供新的靶点.
目的 比較增生性瘢痕(hypertrophic scar,HS)與正常皮膚的基因錶達差異,從分子水平揭示HS的髮病機製,為其臨床防治提供新思路.方法 利用PubMed公共數據庫文獻挖掘HS與正常皮膚的差異錶達基因,確定HS相關基因,併進行蛋白-蛋白相互作用網絡、生物學通路、GeneOntology(基因本體)和功能註釋聚類等生物信息學分析.結果 篩選HS相關基因55箇(上調基因46箇,下調基因9箇).51箇基因構成蛋白-蛋白相互作用網絡,其中上調基因TGFB1、FN1、JUN、COL1A1、CTGF、VEGFA、FOS、COL3A1、IGF1、IL4、PELO、SMAD2、TIMP1、PCNA、ITGA4和下調基因ITGB1和DCN為此網絡中心節點.HS相關基因參與黏著斑形成、整閤素信號轉導和腫瘤相關等生物學通路.併在細胞錶麵受體介導和胞內信號轉導、組織髮育與形態髮生、細胞凋亡與增殖、大分子閤成與代謝等生物過程,鈣離子結閤、雙鏈DNA結閤、啟動子結閤、肝素結閤和促分裂素原活化蛋白激酶(MAPK)激活等分子功能中起著重要作用.功能註釋聚類顯示,HS相關基因多與錶皮組織髮育,血管生成,以及細胞凋亡調控有關.結論 TGFB1、FN1、JUN等關鍵基因,以及錶皮組織髮育,血管生成,以及細胞外基質-整閤素-黏著斑相關的生物學通路、生物學過程和分子功能在HS的髮生髮展中可能起著重要作用,對其進一步分析有利于揭示HS的髮病機製,併為臨床治療提供新的靶點.
목적 비교증생성반흔(hypertrophic scar,HS)여정상피부적기인표체차이,종분자수평게시HS적발병궤제,위기림상방치제공신사로.방법 이용PubMed공공수거고문헌알굴HS여정상피부적차이표체기인,학정HS상관기인,병진행단백-단백상호작용망락、생물학통로、GeneOntology(기인본체)화공능주석취류등생물신식학분석.결과 사선HS상관기인55개(상조기인46개,하조기인9개).51개기인구성단백-단백상호작용망락,기중상조기인TGFB1、FN1、JUN、COL1A1、CTGF、VEGFA、FOS、COL3A1、IGF1、IL4、PELO、SMAD2、TIMP1、PCNA、ITGA4화하조기인ITGB1화DCN위차망락중심절점.HS상관기인삼여점착반형성、정합소신호전도화종류상관등생물학통로.병재세포표면수체개도화포내신호전도、조직발육여형태발생、세포조망여증식、대분자합성여대사등생물과정,개리자결합、쌍련DNA결합、계동자결합、간소결합화촉분렬소원활화단백격매(MAPK)격활등분자공능중기착중요작용.공능주석취류현시,HS상관기인다여표피조직발육,혈관생성,이급세포조망조공유관.결론 TGFB1、FN1、JUN등관건기인,이급표피조직발육,혈관생성,이급세포외기질-정합소-점착반상관적생물학통로、생물학과정화분자공능재HS적발생발전중가능기착중요작용,대기진일보분석유리우게시HS적발병궤제,병위림상치료제공신적파점.
Objective To explore the pathogenesis mechanism of hypertrophic scar (HS) and the effective means for its clinical treatment,the difference of the gene expressions between HS and normal skin was compared.Methods The differentially expressed genes between HS and normal skin were obtained by mining PubMed.The dysregulated genes in HS were analyzed by a series of bioinformatics methods,including protein-protein interaction networks,pathways,Gene Ontology and functional annotation clustering analysis.Results A total of 55 dysregulated genes in HS was identified (46 up-regulated genes and 9 down-regulated genes ).Fifty-one genes were found to encode proteins with interaction network,including up-regulated genes TGFB1,FN1,JUN,COL1A1,CTGF,VEGFA,FOS,COL3A1,IGF1,II4,PELO,SMAD2,TIMP1,PCNA,and ITGA4 and down-regulated genes ITGB1 and DCN as the central nodes for this network.The dysregulated genes in HS involved in a variety of biological pathways,such as focal adhesion formation,integrin signal transduction,and tumor formation.Furthermore,the dysregulated genes in HS played the important roles in biological processes of cell surface receptor linked signal transduction,tissue development,cell proliferation and apoptosis,and macromolecule biosynthetic process,as well as in molecular function of calcium ion binding,double-stranded DNA binding,heparin binding,promoter binding and MAP kinase activity.The results of functional annotation clustering analysis revealed that the dysregulated genes in HS involved in epidermis development,angiogenesis,and apoptosis.Conclusion Such key genes as TGFB1,FN1,and JUN,along with the pathways,biological processes and molecular functions involving epidermis development,angiogenesis,and extracellular matrixintegrin-focal adhesion signal transduction may play the important roles in the development of HS.The investigations of the dysregulated genes in HS could provide the new targets for clinical treatment.
