Slomiany A, Nishikawa H, Slomiany B L
University of Medicine and Dentistry of New Jersey, Research Center, Newark 07103-2400, USA.
J Physiol Pharmacol. 2002 Mar;53(1):21-38.
Performance of mucosal epithelial barrier is modified by numerous agents that exert effects on mucin- Mucin Binding Protein (MBP) complex. The aim ofthe studies described was to determine the nature of the damage or modification of oral mucous barrier by the short-term exposure to ethanol.
Culture of rat buccal mucosa in the presence of ethanol and [3H]-labeled proline and palmitate revealed substantial decrease in MBP synthesis and the release of MBPto the medium. The radioscanning of the samples prepared from the culture medium and the apical epithelial membranes subjected to SDS-PAGE and western blotting disclosed that the released, water soluble 97kDa MBP glycopeptide was labeled with proline and palmitate. When the experiments were conducted in the presence of 5mM EDTA, the GPI-PLD inhibitor, the majority of radiolabeled MBP remained in the membrane-bound form and was extractable with Triton X- 114. The results on the purified GPI-linked MBP degradation by serum enzyme, by the saliva containing serum transudate, and the suppression of the process by inclusion of GPI-PLD-specific inhibitor support our contention that membrane MBP is released to medium by GPI-PLD-like activity.
The release of MBP from apical epithelial surfaces was induced by depletion of mucin and the presence of serum-derived GPI-PLD in the tissue homogenate. Strong likelihood exists that under in situ conditions ethanol-induced transudation of serum to saliva provides the vehicle for the transfer of GPI-PLD activity to salivary contents. Defacement of the oral surfaces from mucous barrier signals prospect of lumenal agent influence on the unprotected epithelial exterior, and allows ingression of microbes and untoward acting substances into the organism.
黏膜上皮屏障的功能会受到多种作用于黏蛋白-黏蛋白结合蛋白（MBP）复合物的因子的影响。本研究的目的是确定短期接触乙醇对口腔黏膜屏障造成的损伤或改变的性质。
在含有乙醇以及[3H]标记的脯氨酸和棕榈酸的条件下培养大鼠颊黏膜，结果显示MBP的合成以及MBP向培养基中的释放显著减少。对培养基和经十二烷基硫酸钠-聚丙烯酰胺凝胶电泳（SDS-PAGE）及蛋白质免疫印迹法处理的顶端上皮细胞膜制备的样本进行放射性扫描发现，释放出的水溶性97kDa MBP糖肽被脯氨酸和棕榈酸标记。当在5mM乙二胺四乙酸（EDTA）（一种糖基磷脂酰肌醇特异性磷脂酶D（GPI-PLD）抑制剂）存在的情况下进行实验时，大多数放射性标记的MBP仍以膜结合形式存在，并且可用曲拉通X-114提取。关于血清酶、含血清渗出液的唾液对纯化的糖基磷脂酰肌醇（GPI）连接的MBP的降解作用以及通过加入GPI-PLD特异性抑制剂对该过程的抑制作用的结果支持了我们的观点，即膜MBP是通过类似GPI-PLD的活性释放到培养基中的。
黏蛋白的消耗以及组织匀浆中血清来源的GPI-PLD的存在诱导了MBP从顶端上皮表面的释放。很有可能在原位条件下，乙醇诱导的血清向唾液的渗出为GPI-PLD活性向唾液成分的转移提供了载体。口腔表面黏膜屏障的破损预示着腔内物质会影响未受保护的上皮外部，并使微生物和有害物质进入机体。
