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尖锐湿疣患者角质形成细胞中活化型细胞外信号调控蛋白激酶和活化型p38的检测 被引量:8

Expression of Activated ERK and p38 Kinase in HPV-Infected Keratinocytes
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摘要 目的探讨尖锐湿疣皮损角质形成细胞中活化型细胞外信号调控蛋白激酶(p-ERK)和活化型p38(p-p38)的表达。方法采用原位杂交方法诊断HPV6/11相关尖锐湿疣50例;采用免疫组化EnVision二步法检测50例尖锐湿疣皮损中p-ERK和p-p38的表达及分布,并以25例正常人皮肤(包皮)作为对照。结果①p-ERK和p-p38在尖锐湿疣角质形成细胞中的表达较正常人上皮中均有不同程度的增强,前者u=4.113,P<0.01;后者u=4.497,P<0.01,其表达主要分布于棘细胞层,阳性信号均定位于胞核。②尖锐湿疣皮损中,p-ERK与p-p38的表达呈显著正相关(r=0.42,P<0.01)。结论HPV6/11阳性尖锐湿疣患者中,p-ERK和p-p38的表达较正常人皮肤明显增强,提示在HPV6/11感染时,角质形成细胞中激酶ERK和p38的激活增加,可能通过ERK和p38MAPK通路起作用。 Objective To investigate the expression of activated ERK (p-ERK) and activated p38 (p-p38) in the keratinocytes of condyloma acuminata (CA) lesions. Methods Fifty cases of HPV 6/11 CA were diagnosed by in situ hybridization. The expression and distribution of p-ERK and p-p38 in CA lesions and 25 normal human skins (foreskins) were detected by immunohistochemistry technique (En Vision). Results ①The results showed that the expression of p-ERK and p-p38 in keratinocytes of CA lesions were significantly higher than those in normal epidermis (P < 0.01), and the expression distributed mainly in prickle layer of CA lesions. The positive signal located mainly in the nuclei. ②In CA lesions the expression of p-ERK and p-p38 was positively correlated. Conclusions The study suggests that, for CA caused by HPV 6/11, both ERK and p38 MAPK may play a role in MAP kinase signaling pathway.
出处 《中华皮肤科杂志》 CAS CSCD 北大核心 2004年第10期569-571,共3页 Chinese Journal of Dermatology
基金 杭州市医药卫生青年研究基金(0203)
关键词 尖锐湿疣 ERK 角质形成细胞 表达 正常人 HPV 患者 激酶 细胞外信号 调控蛋白 Condylomata acuminata Papillomavirus, human Mitogen-activated protein kinase kinases p38
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  • 1Zachos G, Clements B, Conner J. Herpes simplex virus type 1 infection stimulates p38/c-Jun N-terminal mitogen-activated protein kinase pathways and activates transcription factor AP-1. J Biol Chem.1999, 274: 5097-5103.
  • 2Papatsoris AG, Papavassiliou AG. Molecular ′palpation′ of BPH: a tale of MAPK signalling? Trends Mol Med, 2001, 7:288-292.
  • 3Crusius K, Rodriguez I, Alonso A. The human papillomavirus type 16E5 protein modulates ERK1/2 and p38 MAP kinase activation by an EGFR-independent process in stressed human keratinocytes. Virus Genes, 2000, 20: 65-69.

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