高铁培养环境对小鼠前成骨细胞MC3T3-E1增殖、分化的影响

目的 观察高铁培养环境下小鼠前成骨样细胞MC3T3-E1增殖、分化指标的变化趋势,探讨铁离子对 成骨细胞增殖、分化的影响。方法 小鼠前成骨样细胞MC3T3-E1在37℃条件下体外培养,在10mmol/Lβ-甘 油磷酸和50μg /mL抗坏血酸的诱导分化的作用下,分化为成骨细胞,同时用不同浓度(50、100、 200μmol/L)枸橼酸铁铵(FAC)干预,用MTT法检测细胞的增殖活性,RT-PCR法检测成骨细胞分化基因成骨 相关转录因子(Runx2) 、锌指结构转录因子(Osterix) 、骨唾液酸蛋白(BSP)和骨钙素(OC)的表达,碱性 磷酸酶(ALP)活性试剂盒检测细胞碱性磷酸酶活性。结果 MC3T3-E1细胞的增殖活性、成骨分化相关基因的 表达以及ALP水平随FAC干预浓度的增加呈剂量依赖性降低(P<0.05)。结论 高铁培养环境可明显抑制小鼠 前成骨样细胞MC3T3-E1的增殖和分化。     

续苓健骨汤含药血清对MC3T3-E1细胞分化及增殖的影响

目的探讨续苓健骨汤含药血清对MC3T3-E1成骨细胞分化及增殖的影响。方法制备续苓健骨汤含药血清,实验分为空白对照组、含药血清低剂量组、中剂量组和高剂量组。采用CCK-8法和流式细胞术检测续苓健骨汤含药血清对MC3T3-E1细胞增殖和细胞周期的影响;碱性磷酸酶(ALP)活性测定MC3T3-E1细胞的成骨分化能力;茜素红染色检测MC3T3-E1细胞的矿化能力;实时荧光定量PCR检测成骨分化基因Runx2、OC、Bmp2、Col1a1mRNA水平。结果与空白对照组比较,中、高剂量续苓健骨汤含药血清能促进MC3T3-E1细胞增殖、S期细胞比率和细胞增殖指数,并且呈现一定的剂量依赖性;同时中高剂量续苓健骨汤含药血清组能明显提高MC3T3-E1细胞ALP活性(P0.01)和钙化能力(P0.01),促进Runx2、OC、Bmp2、Col1a1 mRNA的表达(P0.05)。结论续苓健骨汤含药血清能促进成骨细胞MC3T3-E1的增殖,并通过上调骨形成相关基因Runx2、OC、BMP2、Col1a1的表达水平,提高MC3T3-E1细胞的成骨能力。     

黄瓜籽总皂苷对MC3T3-E1细胞分化及SPARC、OPG/RANKL表达的影响

目的观察黄瓜籽总皂苷提取物(cucumber seed saponins,CSS)对小鼠成骨细胞MC3T3-E1增殖、分化和矿化的影响,以及与骨质疏松相关的SPARC、OPG/RANKL/RANK信号通路的作用。方法通过MTT实验、碱性磷酸酶(alkaline phosphatase,ALP)活性检测、茜素红染色,考察不同浓度CSS对MC3T3-E1细胞增殖、分化及矿化的影响;采用RT-PCR方法检测SPARC、OPG/RANKL mRNA表达水平; Western blot检测SPARC、OPG/RANKL的蛋白表达量。结果与阳性对照组相比,CSS能明显促进MC3T3-E1细胞增殖(P0.05),CSS高、中剂量组能明显提高MC3T3-E1细胞ALP活性及钙化结节数量(P0.05);与空白组相比,CSS不同剂量组均明显上调SPARC、OPG/RANKL mRNA及蛋白表达水平(P0.05)。结论黄瓜籽总皂苷能够促进成骨细胞MC3T3-E1的增殖、分化及矿化能力,并通过上调SPARC、OPG/RANKL的表达水平提高MC3T3-E1细胞的成骨能力。     

信号分子p38参与低频脉冲电磁场促进成骨细胞矿化成熟的实验研究

目的研究信号分子丝裂原活化蛋白激酶(mitogen-activated protein kinases,MAPKs)是否参与50 Hz、0.6 m T低频脉冲电磁场促进大鼠颅骨成骨细胞矿化成熟的过程。方法取出生48 h内的SPF级Wistar大鼠6只,采用酶消化法分离培养大鼠颅骨成骨细胞。取原代颅骨成骨细胞,经50 Hz、0.6 m T低频脉冲电磁场处理0、5、10、20、40、60、120 min后,采用Western blot检测MAPKs的磷酸化水平。将成骨细胞随机分为对照组(A组)、低频脉冲电磁场处理组(B组)、p-p38抑制剂SB202190组(C组)、SB202190+低频脉冲电磁场处理组(D组),经相应处理1、4、7 d后检测其ALP活性。将90%以上融合的成骨细胞经成骨诱导处理后同上法分组,处理9 d时行ALP组织化学染色,12 d时行茜素红染色观察。结果 Western blot检测示,处理各时间点磷酸化细胞外信号调节激酶1/2、磷酸化c-Jun氨基末端激酶1/2蛋白表达量无显著变化(P0.05);而p-p38蛋白表达量则在处理5 min后开始升高,至40 min时达峰值,之后开始逐步下降,但各时间点均显著高于0 min时(P0.05)。B组ALP活性、ALP阳性克隆数、ALP阳性克隆面积、钙结节数及钙结节面积均显著多于A、C、D组(P0.05)。结论在50 Hz、0.6 m T低频脉冲电磁场促进大鼠颅骨成骨细胞矿化成熟的过程中,信号分子p38参与其中。     

红车轴草总异黄酮含药血清对MC3T3-E1细胞增殖、分化和矿化的影响

目的研究红车轴草总异黄酮含药血清对MC3T3-E1成骨样细胞增殖、分化和矿化的影响。方法大鼠灌胃红车轴草总异黄酮一定时间后,制备含药血清,并分别采用MTT法、碱性磷酸酶活性测定法、ELISA法和茜素红染色测定矿化结节的方法考察不同浓度红车轴草总异黄酮含药血清对MC3T3-E1成骨样细胞的增殖率、碱性磷酸酶活性、骨钙素生成以及矿化结节形成的影响。结果不同浓度的红车轴草总异黄酮含药血清都能显著促进MC3T3-E1成骨样细胞的增殖并显著提高MC3T3-E1成骨样细胞碱性磷酸酶的活性,且最佳的含药血清浓度为5%;5%的红车轴草总异黄酮含药血清处理MC3T3-E1成骨样细胞6 d和9 d可显著促进骨钙素的分泌;5%的红车轴草总异黄酮含药血清处理MC3T3-E1成骨样细胞6 d、12 d和18 d,形成的矿化结节均显著高于对照组。结论红车轴草总异黄酮含药血清可以显著促进MC3T3-E1成骨样细胞的增殖、碱性磷酸酶活性、骨钙素分泌和矿化,说明红车轴草总异黄酮含药血清确实可以促进MC3T3-E1成骨样细胞的分化成熟,该药物具有开发为抗骨质疏松症新药的潜力。     

镁锌合金在体外对MC3T3-E1细胞增殖、分化和矿化的影响

目的 观察镁锌合金(Mg-zn)在体外的降解及对小鼠前成骨细胞(MC313-E1)增殖、分化和矿化的影响,探讨Mg-Zn成为新型骨科内植物材料的可行性.方法 Mg-Zn和纯镁(Mg)试样置入模拟体液(SBF)中,3 d后通过电化学方法和静态浸泡失重的方法来测定其腐蚀电位及腐蚀速率;在Mg-Zn上接种MC3T3-E1细胞,采用噻唑蓝(MTT)比色法检测1、3、5、7、9 d时细胞增殖活性,采用碱性磷酸酶(ALP)检测试剂盒检测14、28 d时细胞ALP活性,并用四环素荧光染色检测14d时矿化结节.与左旋聚乳酸(PLLA)作对照研究.结果 Mg-Zn的腐蚀电位增高,腐蚀速率降低;培养第5、7、9天后,Mg-Zn成骨细胞增殖活性明显高于PLLA(P<0.01);14、28 d时,Mg-Zn ALP活性明显高于PuA(P<0.01);Mg-Zn矿化结节面积明显大于PLLA(P<0.01).结论 Mg-Zn明显改善了Mg的耐腐蚀性能,同时能促进MC333-E1细胞的增殖、分化和矿化功能,具有良好的生物相容性.     

镁锌合金在体外对MC3T3-E1细胞增殖、分化和矿化的影响

目的 观察镁锌合金(Mg-zn)在体外的降解及对小鼠前成骨细胞(MC313-E1)增殖、分化和矿化的影响,探讨Mg-Zn成为新型骨科内植物材料的可行性.方法 Mg-Zn和纯镁(Mg)试样置入模拟体液(SBF)中,3 d后通过电化学方法和静态浸泡失重的方法来测定其腐蚀电位及腐蚀速率;在Mg-Zn上接种MC3T3-E1细胞,采用噻唑蓝(MTT)比色法检测1、3、5、7、9 d时细胞增殖活性,采用碱性磷酸酶(ALP)检测试剂盒检测14、28 d时细胞ALP活性,并用四环素荧光染色检测14d时矿化结节.与左旋聚乳酸(PLLA)作对照研究.结果 Mg-Zn的腐蚀电位增高,腐蚀速率降低;培养第5、7、9天后,Mg-Zn成骨细胞增殖活性明显高于PLLA(P<0.01);14、28 d时,Mg-Zn ALP活性明显高于PuA(P<0.01);Mg-Zn矿化结节面积明显大于PLLA(P<0.01).结论 Mg-Zn明显改善了Mg的耐腐蚀性能,同时能促进MC333-E1细胞的增殖、分化和矿化功能,具有良好的生物相容性.     

镁锌合金在体外对MC3T3-E1细胞增殖、分化和矿化的影响

目的 观察镁锌合金(Mg-zn)在体外的降解及对小鼠前成骨细胞(MC313-E1)增殖、分化和矿化的影响,探讨Mg-Zn成为新型骨科内植物材料的可行性.方法 Mg-Zn和纯镁(Mg)试样置入模拟体液(SBF)中,3 d后通过电化学方法和静态浸泡失重的方法来测定其腐蚀电位及腐蚀速率;在Mg-Zn上接种MC3T3-E1细胞,采用噻唑蓝(MTT)比色法检测1、3、5、7、9 d时细胞增殖活性,采用碱性磷酸酶(ALP)检测试剂盒检测14、28 d时细胞ALP活性,并用四环素荧光染色检测14d时矿化结节.与左旋聚乳酸(PLLA)作对照研究.结果 Mg-Zn的腐蚀电位增高,腐蚀速率降低;培养第5、7、9天后,Mg-Zn成骨细胞增殖活性明显高于PLLA(P<0.01);14、28 d时,Mg-Zn ALP活性明显高于PuA(P<0.01);Mg-Zn矿化结节面积明显大于PLLA(P<0.01).结论 Mg-Zn明显改善了Mg的耐腐蚀性能,同时能促进MC333-E1细胞的增殖、分化和矿化功能,具有良好的生物相容性.     

不同强度正弦交变磁场对体外培养成骨细胞增殖与分化影响

目的研究频率为50Hz的不同强度正弦交变电磁场对体外培养成骨细胞(Osteoblasts,OB)的影响。方法原代培养大鼠颅骨成骨细胞,传代后随机分为9组,每组分别暴露在频率50Hz,磁场强度为0(对照组)、0.9、1.2、1.5、1.8、2.1、2.4、2.7、3.0mT的正弦交变磁场中,30min/次/d。倒置相差显微镜下观察细胞形态,48h后测定细胞增殖情况,第3、6、9、12、15d测定碱性磷酸酶(Alkaline Phosphatase,ALP)活性,第10d进行ALP组织化学染色,第12d进行茜素红钙化结节染色。结果成骨细胞于磁场暴露处理3d～4d后呈漩涡样分布;与对照组相比,0.9、1.2、1.5、1.8、2.1、2.7和3.0mT组均显著抑制细胞增殖(P0.01或P0.05),2.4mT组无明显影响(P0.05);除3.0mT组外,其它各组的ALP活性均高于对照组(P0.05),尤以1.8mT组最高(P0.01);1.2、1.5、1.8、2.1和2.4mT组的ALP阳性克隆数明显多于对照组,1.8mT组最多,0.9、2.7和3.0mT组与对照组无明显差别;茜素红钙化结节计数结果与ALP组织化学染色结果的趋势相一致。结论 50Hz,0.9mT～3.0mT的正弦交变磁场(2.4mT除外)均抑制体外培养成骨细胞的增殖,但能促进其分化成熟与钙化,尤以1.8mT效果最为明显。     

不同浓度rhBMP-2对MC3T3-E1细胞增殖、ALP活性及成骨分化的影响

目的研究不同浓度rh BMP-2对MC3T3-E1细胞增殖、ALP活性及成骨分化的影响规律。方法 MC3T3-E1细胞接种到培养板24 h后,试验组分别加入1.25、2.5、5、10μg/ml的rh BMP-2进行药物干预,对照组加入全培。试验组应用CCK-8法检测细胞增殖活性,PNPP法检测细胞ALP活性,RT-PCR法检测成骨标志蛋白m RNA的表达情况。结果rh BMP-2浓度为2.5μg/ml时开始促进细胞的增殖(P0.05),rh BMP-2浓度为5μg/ml时促进作用达到峰值(P0.05)。rh BMP-2浓度为2.5μg/ml时ALP活性显著提高(P0.05);rh BMP-2浓度为5μg/ml和10μg/ml时,ALP活性较浓度为2.5μg/ml时继续升高,但差异无统计学意义(P0.05)。ALP、COL1-α以及转录因子RUNX-2的m RNA含量均在加入浓度5μg/ml rh BMP-2后明显升高(P0.05),继续加大rh BMP-2浓度,m RNA含量没有明显增加。结论在研究范围内,rh BMP-2对MC3T3-E1的影响呈浓度依赖性。     

pcDNA3-hBMP2转染对成纤维细胞 生物学性状的影响

目的 探讨人BMP2基因转染对成纤维细胞NIH3T3生物学性状的影响。方法 构建重组真核表达载体pcDNA3-hBMP2,并在脂质体介导下,将其导入NIH3T3成纤维细胞,通过G418筛选获得阳性克隆,用细胞原位杂交和免疫组织化学方法检测hBMP2基因在NIH3T3成纤维细胞内的表达情况;MTT法和FCM检测pcDNA3-hBMP2转染pcDNA3-hBMP2后成纤维细胞超微结构的改变,碱性磷酸酶的检测观察转染pcDNA3-hBMP2后成纤维细胞向成骨细胞分化情况。结果 转染pcvDNA3-hBMP2后的NIH3T3细胞内有大量hBMP2mRNA的转录及其蛋白的表达;转染pcDNA3-hBMP2对成纤维细胞增殖和细胞周期无影响;转染pcDNA3-hBMP2后的成纤维细胞超微结构可见粗面内质网丰富,囊腔扩张明显其内充满中等电子密度的蛋白分泌物;碱性磷酸酶活性显著上升。结论 pcDNA3-hBMP2转染对成纤维细胞NIH3T3增殖和细胞周期无影响。转染后的成纤维细胞不仅可形成BMP2,而且具有向成骨细胞系分化的特性。     

Choledochal cysts: Part 3 of 3: Management

Much about the etiology, pathophysiology, natural course and optimal treatment of cystic disease of the biliary tree remains under debate. Gastroenterologists, surgeons and radiologists alike still strive to optimize their roles in the management of choledochal cysts. To that end, much has been written about this disease entity, and the purpose of this 3-part review is to organize the available literature and present the various theories currently argued by the experts. In part 3, we discuss the management of choledochal cysts, thus completing our comprehensive review.     

H3K4m3和H3K9m3修饰对胰岛组织特异性基因表达的影响

目的 通过比较不同细胞类型之间胰腺十二指肠同源盒1(Pdx-1)、配对盒基因4(Pax4)、MafA(mast cell function associated antigen)和Nkx6.1等胰岛组织特异性基因其转录起始区的H3K4m3和H3K9m3修饰的差异,探讨H3K4m3和H3K9m3修饰对胰岛组织特异性基因表达的作用.方法 采用染色质免疫共沉淀一实时定量聚合酶链反应(PCR)法检测小鼠胚胎干细胞(mES,1×10~7)、小鼠成纤维细胞株NIH3T3细胞(1×10~7)和小鼠β细胞株NIT-1细胞(1×10~7)三者中的胰岛组织特异性基因、Oct4基因和MLH1基因转录起始区H3K4m3和H3K9m3修饰的状况.同时采用实时定量逆转录(RT)-PCR检测上述3种细胞各基因mRNA表达水平.分析H3K4m3和H3K9m3修饰改变与基因表达之间的关系.结果 NIT-1细胞中Pdx-1、Pax4、MafA、Nkx6.1等胰岛组织特异性基因转录起始区的H3K4m的修饰水平分别为:(4.84±0.05)%、(9.91±1.33)%、(10.64±0.87)%、(0.23±0.03)%,与mES细胞比较明显增高(P<0.05),基因表达;NIH3T3细胞中Pdx-1、Pax4、MafA、Nkx6.1等胰岛组织特异性基因转录起始区的H3K9m3的修饰水平分别为:(0.64±0.21)%、(7.04±1.29)%、(0.39±0.10)%、(2.35±0.81)%,与mES细胞比较明显增高(P<0.05),基因不表达.结论 H3K4m3与H3K9m3修饰能相互协调,共同调控胰岛组织特异性基因的表达.     

Overexpression of EIF3S3 promotes cancer cell growth

BACKGROUND: Amplification and overexpression of EIF3S3 gene has been demonstrated in breast and prostate cancer. Here, our goal was to study the effect of EIF3S3 on cell growth. METHODS: The effect of EIF3S3 on growth of NIH 3T3 murine fibroblasts as well as breast (SK-Br-3 and ZR-75-1) and prostate (PC-3 and LNCaP) cancer cell lines was examined by using transfection with inducible pTet-Off system and siRNAs. RESULTS: NIH 3T3 cells with overexpression of EIF3S3 grew significantly faster than cells transfected with empty vector and survived longer when grown in soft agar. The EIF3S3 overexpression was associated with increased fraction of cells in S-phase and with phosphorylation of retinoblastoma (Rb) protein. siRNA treatment inhibited significantly (P = 0.0022) the growth of all breast and prostate cancer cell lines studied. CONCLUSIONS: The results suggest that EIF3S3 regulates cell growth and viability, and that overexpression of the gene may provide growth advantage to the cancer cells.     

Identification of the insulin-regulated interaction of phosphodiesterase 3B with 14-3-3 beta protein

Phosphodiesterase (PDE)-3B, a major PDE isoform in adipocytes, plays a pivotal role in the antilipolytic action of insulin. Insulin-induced phosphorylation and activation of PDE3B is phosphatidylinositol 3-kinase (PI3-K) and Akt dependent, but the precise mechanism of PDE3B activation is not fully understood. We have identified 14-3-3 beta, a critical scaffolding molecule in signal transduction, as a protein that interacts with PDE3B using the yeast two-hybrid system. The interaction between PDE3B and 14-3-3 beta was then confirmed in vitro. The glutathione S-transferase (GST)-tagged 14-3-3 beta interacts with endogenous PDE3B of rat adipocytes, and this interaction is enhanced when adipocytes are treated with insulin. Coimmunoprecipitation experiments reveal that endogenous PDE3B also associates with endogenous 14-3-3 beta in rat adipocytes, and this interaction is enhanced by insulin. Two different PI3-K inhibitors, wortmannin and Ly294002, block this induction, suggesting that PI3-K is required. Synthetic 15 amino acid peptides of rat PDE3B containing phosphorylated Ser-279 or -302 inhibit this interaction, indicating that the insulin-regulated phosphorylation of these serine residues is involved. Because insulin receptor substrate-1 also associates with 14-3-3, the dimeric 14-3-3 beta could function as a scaffolding protein in the activation of PDE3B by insulin.     

Effects of carboxy-terminal modifications of proteinase 3 (PR3) on the recognition by PR3-ANCA

BACKGROUND: Autoantibodies directed against neutrophil proteinase 3 (PR3-ANCA) from patients with Wegener's granulomatosis and microscopic polyangiitis recognize conformational epitopes of PR3. During maturation of neutrophils, PR3 undergoes amino-terminal and carboxy-terminal processing. In contrast to amino-terminal processing, the effects of carboxy-terminal processing on recognition of PR3 by PR3-ANCA remain unknown. Carboxy-terminally modified or tagged recombinant PR3 (rPR3) molecules may be useful for the refinement of diagnostic assays and for the study of biological processes. METHODS: This study was designed to determine whether 293 cells can be used to express specifically designed carboxy-terminal variants of rPR3, and to evaluate the effects of different carboxy-terminal modifications on the recognition by PR3-ANCA in the capture ELISA. RESULTS: The rPR3-variants secreted into the media supernatants of transfected 293 cells escaped proteolytic processing. Furthermore, in contrast to the effects of amino-terminal pro-peptide deletion on PR3-ANCA binding, carboxy-terminal modifications (deletion and additions) did not significantly affect recognition by PR3-ANCA. CONCLUSIONS: This expression system is ideally suited for the expression of custom-designed carboxy-terminal rPR3 variants, and major conformational effects of carboxy-terminal modifications seem unlikely.     

SH3BP2 mutations potentiate osteoclastogenesis via PLCγ

To determine the mechanism for the increased osteoclastogenesis in the jaw of cherubism patients with SH3BP2 mutations we evaluated the effect of mutant compared to wild‐type SH3BP2 on activation of osteoclast signaling pathways. Indeed mutant forms of SH3BP2 do induce greater osteoclastogenesis. Heterozygous activating mutations in exon 9 of SH3BP2 have been found in most patients with cherubism, an unusual genetic syndrome characterized by excessive remodeling of the mandible and maxilla due to spontaneous and excessive osteoclastic bone resorption. Here we have investigated the functional consequences of SH3BP2 mutations on sRANKL‐induced osteoclastogenesis in RAW 264.7 pre‐osteoclast cells. sRANKL‐stimulated RAW 264.7 cells were transfected with wild‐type or mutant SH3BP2 plasmids. NFAT‐luciferase and tartrate resistant acid phosphatase (TRAP), a marker of osteoclastic differentiation, levels were evaluated. Western immunoblots were also performed to determine phosphorylation of key proteins involved in the PI‐PLC pathway leading to NFATc1 translocation. Our results indicate that forced expression of mutant forms of SH3BP2, found in cherubism patients, in RAW 264.7 cells induce greater NFAT activity and greater expression of TRAP than forced expression of wild‐type SH3BP2. These findings indicate that missense SH3BP2 mutations cause a gain of protein function. Moreover, over expression of SH3BP2 in RAW 264.7 cells potentiates sRANKL‐stimulated phosphorylation of PLCγ1 and PLCγ2. Our studies demonstrate that cherubism is due to gain‐of‐function mutations in SH3BP2 that stimulate RANKL‐induced activation of PLCγ. The consequent activation of calcineurin and NFAT proteins induces the excessive osteoclastic phenotype of cherubism. © 2010 Orthopaedic Research Society. Published by Wiley Periodicals, Inc. J Orthop Res 28:1425–1430, 2010     

Actin and microtubule cytoskeletons of the processes of 3D-cultured MC3T3-E1 cells and osteocytes

Cell shape is the most critical determinant of cell function and is potentially influenced by the organization of a cell's cytoskeletal components. It has been reported that three-dimensionally cultured osteoblasts have a morphology that closely resembles that of osteocytes, most notably including formation of processes. We have previously shown the critical differences between cytoskeletal components in osteoblasts and osteocytes in two-dimensional culture. We have now extended that investigation to the cytoskeletal components of 3D-cultured osteoblasts and osteocytes using 3D cultures of the osteoblast cell line, MC3T3-E1, and primary osteocytes grown in collagen gel. Three-dimensional fluorescent image reconstructions for actin, fimbrin, alpha-actinin, myosin, tropomyosin, and microtubules were made using IMARIS software. Actin, fimbrin, alpha-actinin, myosin, and tropomyosin all appeared in the processes of both cell types, but fimbrin and myosin showed differences in their distribution patterns between cell types. Microtubules were limited in distribution to the proximal region of osteocyte processes but extended the entire length of MC3T3-E1 cell processes. Microtubules were essential for the integrity and formation of MC3T3-E1 cell processes, but osteocyte processes were dependent on actin. These results showed that there are significant differences between the actin and microtubule cytoskeletons in the processes of 3D-cultured MC3T3-E1 cells and in the processes of 3D-cultured primary osteocytes. These differences in the cytoskeleton of the processes of 3D-cultured osteoblasts and of osteocyte dendrites suggest that osteoblast processes may have a different functional role than the osteocyte dendritic network. An erratum to this article is available at .     

Expression of p63 and 14-3-3σ in normal and hyperdifferentiated mucosa of the upper aerodigestive tract

Objective: Our goal was to analyze p63 and 14-3-3σ expression in normal and hyperdifferentiated head and neck mucosa. Study Design: Compare the in vivo expression of p63 and 14-3-3σ by immunohistochemistry in normal mucosa and oral lichen planus, a benign mucosal lesion marked by hyperdifferentiation and apoptosis. Results and Conclusion: p63 is underexpressed and 14-3-3σ is overexpressed in lichen planus on immunohistochemical analysis. Significance: The findings support the hypothesis that p63 plays an antidifferentiation role, whereas 14-3-3σ plays a prodifferentiation role in the upper aerodigestive tract epithelium. Lichen planus is a valuable model for the study of p63, 14-3-3σ, and mucosal differentiation. p63 and 14-3-3σ may be molecular markers for oral lichen planus. (Otolaryngol Head Neck Surg 2002;126:598-601.)