Department of Otolaryngology, Vanderbilt University Bill Wilkerson Center for Otolaryngology and Communication Sciences, Nashville, Tennessee 37232-4480, USA.
Laryngoscope. 2011 Feb;121(2):346-51. doi: 10.1002/lary.21364. Epub 2011 Jan 13.
OBJECTIVES/HYPOTHESIS: We investigated the hypothesis that 30 minutes of raised intensity phonation alters transcript levels of vocal fold intercellular tight junction proteins and disrupts the vocal fold epithelial barrier.
Prospective animal study.
Eighteen New Zealand white breeder rabbits were randomly assigned to receive 30 minutes of raised intensity phonation or approximation of the vocal folds without phonation. Quantitative polymerase chain reaction (qPCR) was used to investigate transcript levels of the epithelial intercellular tight junction proteins, occludin and zonula occludin-1 (ZO-1), and the adherens junction proteins β-catenin and E-cadherin. Structural alterations to the vocal fold epithelium were further examined by scanning electron microscopy (SEM) and transmission electron microscopy (TEM).
Mann-Whitney U revealed significantly decreased occludin (P = .016) and β-catenin (P = .016) gene expression from rabbits undergoing raised intensity phonation compared with control. There were no significant differences in Z0-1 and E-cadherin gene expression between groups (P > .025). SEM revealed significant obliteration, desquamation, and evidence of microhole formation in rabbit vocal folds exposed to raised intensity phonation compared with control, whereas TEM revealed dilated intercellular morphology between groups.
Results provide support for the hypothesis that a transient episode of raised intensity phonation alters transcript levels of vocal fold intercellular tight junction proteins and disrupts integrity of the epithelial barrier. The loss of barrier integrity may have significant consequences on epithelial defenses and compromise protection of the underlying mucosa from damage secondary to prolonged vibration exposure.
目的/假设：我们研究了以下假设：30 分钟的高强度发声会改变声带细胞间紧密连接蛋白的转录水平，并破坏声带上皮屏障。
前瞻性动物研究。
将 18 只新西兰白种繁殖兔随机分为接受 30 分钟高强度发声或接近声带但不发声两组。采用实时定量聚合酶链反应（qPCR）检测上皮细胞间紧密连接蛋白Occludin 和 Zonula Occludin-1（ZO-1），以及黏着连接蛋白β-连环蛋白（β-catenin）和 E-钙黏蛋白（E-cadherin）的转录水平。通过扫描电子显微镜（SEM）和透射电子显微镜（TEM）进一步观察声带上皮的结构变化。
Mann-Whitney U 检验显示，与对照组相比，接受高强度发声的兔的 Occludin（P=0.016）和β-catenin（P=0.016）基因表达显著降低。ZO-1 和 E-cadherin 基因表达在两组间无显著差异（P>0.025）。SEM 显示，与对照组相比，接受高强度发声的兔的声带出现明显的闭塞、脱落和微孔形成的证据，而 TEM 显示两组间细胞间形态扩张。
结果支持以下假设：短暂的高强度发声会改变声带细胞间紧密连接蛋白的转录水平，并破坏上皮屏障的完整性。屏障完整性的丧失可能会对上皮防御产生重大影响，并在长时间振动暴露导致的黏膜损伤方面损害对潜在黏膜的保护。
