Effects of high mobility group protein box 1 and toll like receptor 4 pathway on warts caused by human papillomavirus.
Effects of high mobility group protein box 1 and toll like receptor 4 pathway on warts caused by human papillomavirus.
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高迁移率族蛋白盒1和Toll样受体4通路对人乳头瘤病毒引起的疣的影响
DOI：
10.3892/mmr.2014.2477
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发表时间：
2014-10
影响因子：
3.4
通讯作者：
Shen G
中科院分区：
文献类型：
--
作者：
Weng H;Liu H;Deng Y;Xie Y;Shen G
越来越多的证据表明，炎症在人乳头瘤病毒（HPV）致瘤性中具有重要作用。然而，高迁移率族蛋白盒1（HMGB 1）-Toll样受体4（TLR 4）信号通路相关炎症对HPV引起的表皮疣的影响尚不清楚。本研究探讨HMGB 1、TLR 4和核因子-κB p65在尖锐湿疣（CA）和寻常疣（VV）中的表达。免疫组化和westernblot分析显示，VV和CA上皮细胞核中p65的表达均显著高于正常皮肤（P<0.01），CA中p65的表达高于VV，但差异无显著性。细胞外HMGB 1水平从NS到VV再到CA呈进行性升高（P<0.05）。CA组上皮细胞膜表面TLR 4水平显著高于NS组（P<0.01），VV组TLR 4水平显著低于NS组（P<0.01）。上皮细胞核中p65的表达与上皮细胞间隙中HMGB 1的表达呈正相关（r=0.5199，P<0.01）。这些发现表明，炎症在HPV引起的疣中加剧。因此，HMGB 1-TLR 4通路相关炎症可能在CA中起关键作用。HMGB 1而不是TLR 4可能是VV中炎症的重要介质。针对HMGB 1的治疗可能是治疗HPV相关疣的潜在策略。
Accumulative evidence has demonstrated that inflammation has an important role in human papillomavirus (HPV) oncogenicity. However, the effects of high mobility group protein box 1 (HMGB1)-toll like receptor 4 (TLR4) signaling pathway associated inflammation on epidermal warts caused by HPV remain unclear. The present study investigated the HMGB1, TLR4 and nuclear factor-κB p65 expression in condyloma acuminatum (CA) and verruca vulgaris (VV). Immunohistochemistry and western blot analysis revealed that p65 expression in epithelial nuclei in VV and CA was significantly higher than in normal skin (NS) (P<0.01), and p65 in CA was higher than in VV but this difference was not significant. The level of extracellular HMGB1 increased significantly and progressively from NS to VV to CA (P<0.05). The level of TLR4 on the surface of epithelial membranes in the CA samples was significantly higher than in NS (P<0.01), and TLR4 in VV samples was significantly lower than in NS (P<0.01). There was a positive correlation between p65 expression in the epithelial nuclei and HMGB1 in the epithelial intercellular spaces (r=0.5199, P<0.01). These findings indicate that inflammation is intensified in warts caused by HPV. HMGB1-TLR4 pathway-associated inflammation may therefore have a pivotal role in CA. HMGB1, rather than TLR4, may be a vital mediator of inflammation in VV. Therapies targeting HMGB1 may be a potential strategy for the treatment of HPV-associated warts.
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影响因子：
4.8
作者：
Dai, Shipan;Sodhi, Chhinder;Hackam, David J.
通讯作者：
Hackam, David J.
影响因子：
5.7
作者：
Tadie, Jean-Marc;Bae, Hong-Beom;Zmijewski, Jaroslaw W.
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影响因子：
3.9
作者：
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通讯作者：
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影响因子：
5.3
作者：
Poser, I;Golob, M;Bosserhoff, AK
通讯作者：
Bosserhoff, AK
影响因子：
3.8
作者：
Weng H;Deng Y;Xie Y;Liu H;Gong F
通讯作者：
Gong F