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增生性瘢痕中细胞外信号调节激酶及其激酶基因表达的变化 被引量:1

Gene expression of extracellular-signal regulated protein kinase1/2 and their MAPKKs in hypertrophic scars
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摘要 目的 :探讨细胞外信号调节激酶 1/ 2 (extracellular signal regulated protein kinase,ERK1/ 2 )及其上游信号分子 MEK1/ 2在增生性瘢痕和正常皮肤中基因表达的变化。方法 :提取 8例增生性瘢痕和 8例正常皮肤组织的总 RNA后 ,分离 m RNA,用逆转录聚合酶链反应 (RT PCR)法检测这 4种基因在不同组织中的表达变化规律。结果 :在正常皮肤组织中 ,MEK1、MEK2、ERK1和 ERK2基因表达较弱 ;而在增生性瘢痕中 ,这 4种基因表达明显增强 ,其 m RNA量的灰度比分别为正常皮肤的 1.1倍、1.2倍、2 .2倍和 2 .5倍。结论 :增生性瘢痕的发生可能与 MEK1/ 2和 ERK1/ 2基因表达升高有关。 Objective:To explore the change of extracellularsignal regulated protein kinase1/2 (ERK1/2) and their mitogen activated protein kinase kinases(MAPKKs) gene expression in normal skins versus hypertrophic scars underling their biological significances.Methods:After total RNAs were isolated from 8 specimens of hypertrophic scars and 8 specimens of normal skins,and then were purified to mRNAs, the gene expression of ERK1/2 and MEK1/2 were examined with reverse transcriptionpolymerase chain reaction (RTPCR). Results:In normal skins,the intensity of gene expression of ERK1/2 and MEK1/2 were weak .In hypertrophic scar,the expression intensities of these 4 genes were 1.1 times,1.2 times, 2.2 times and 2.5 times of normal skins,respectively.The expression of these 4 genes was significantly elevated in comparison with normal skins.Conclusion:The activation of MEK1/2,ERK1/2 gene expression in hypertrophic scars versus in normal skins might be one of the mechanisms controlling the formation of hypertrophic scars.
出处 《中国危重病急救医学》 CAS CSCD 2003年第4期200-203,共4页 Chinese Critical Care Medicine
基金 国家重大基础研究规划资助项目 ( G19990 5 42 0 4) 国家杰出青年科学基金资助项目 ( 3 95 2 5 0 2 4) 国家自然科学基金资助项目 ( 3 9870 73 1)
关键词 细胞外信号调节激酶1/2 MEK1基因 MEK2基因 增生性瘢痕 extracellularsignal regulated protein kinase1/2 MEK1 gene MEK2 gene hypertrophic scar
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  • 1Tortorella LL, Milasincic DJ, Pilch PF. Critical proliferation independent window for basic fibroblast growth factor repression of myogenesis via the p42/p44 MAPK signaling pathway. J Biol Chem, 2001, 276:13709
  • 2Ravanti L, Toriseva M, Penttinen R et al. Expression of human collagenase-3 (MMP-13) by fetal skin fibroblasts is induced by transforming growth factor beta via p38 mitogen-activated protein kinase. FASEB J,2001,15(6): 1098
  • 3Tournier C, Dong C, Turner TK et al. MKK7 is an essential component of the jnk signal transduction pathway activated by proinflammatory cytokines. Genes Dev, 2001, 15:1419
  • 4Deacon K, Blank JL. Characterization of the mitogen-activated protein kinase kinase 4 (MKK4)/c-Jun NH2-terminal kinase 1 and MKK3/p38pathways regulated by MEK kinases 2 and 3. MEK kinase 3 activates MKK3 but does not cause activation of p38 kinase in vivo
  • 5Seger R, Krebs EG. The MAPK signaling cascade. FASEBJ, 1995,9:726
  • 6Dziareke R, JinYP, Gupta D. Differential activation of extracellular sig nal-regulated kinase (erk)1, erk2, p38 and c-Jun N-terminal kinase mitogen-activated protein kinases by bacterial peptidoglycan. J Infect Dis,1996,174:777
  • 7陈伟,付小兵,孙晓庆,赵志力,周岗,孙同柱,盛志勇.增生性瘢痕内p38丝裂素活化蛋白激酶及其MAPKKs基因的表达[J].解放军医学杂志,2003,28(7):592-593. 被引量:3
  • 8陈伟,付小兵,葛世丽,姜笃银,周岗,孙同柱,盛志勇.胎儿和少儿皮肤内EGF、c-fos和c-myc基因表达变化研究[J].解放军医学杂志,2004,29(4):320-323. 被引量:3

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