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首页> 外文期刊>American Journal of Physiology >Altered phenotype of cultured urothelial and other stratified epithelial cells: implications for wound healing.
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Altered phenotype of cultured urothelial and other stratified epithelial cells: implications for wound healing.

机译：培养的尿路上皮和其他分层上皮细胞的表型改变：对伤口愈合的影响。

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The differentiation of cultured stratified epithelial cells can deviate significantly from that of normal epithelium, leading to suggestions that cultured cells undergo abnormal differentiation, or a truncated differentiation. Thus cultured epidermal and corneal epithelial cells stop synthesizing their tissue-specific keratin pair K1/K10 and K3/K12, respectively. The replacement of these keratins in the suprabasal compartment by K6/K16 keratins that are made by all stratified squamous epithelia during hyperplasia rules out a truncated differentiation. Importantly, the keratin pattern of in vivo corneal epithelium undergoing wound repair mimics that of cultured rabbit corneal epithelial cells. Although cultured urothelial cells continue to synthesize uroplakins, which normally form two-dimensional crystalline urothelial plaques covering almost the entire apical urothelial surface, these proteins do not assemble into crystals in cultured cells. Cultured epithelial cells can, however, rapidly regain normal differentiation on the removal of mitogenic stimuli, the use of a suitable extracellular matrix, or the transplantation of the cells to an in vivo, nonmitogenic environment. These data suggest that cultured epithelial cells adopt altered differentiation patterns mimicking in vivo regenerating or hyperplastic epithelia. Blocking the synthesis of tissue-specific differentiation products, such as the K1 and K10 keratins designed to form extensive disulfide cross-links in cornified cells, or the assembly of uroplakin plaques allows epithelial cells to better migrate and proliferate, activities that are of overriding importance during wound repair. Cultured urothelial and other stratified epithelial cells provide excellent models for studying the regulation of the synthesis and assembly of differentiation products, a key cellular process during epithelial wound repair.
机译：培养的分层上皮细胞的分化可能与正常上皮的分化明显不同，从而提示培养的细胞经历异常分化或截短的分化。因此，培养的表皮和角膜上皮细胞分别停止合成其组织特异性角蛋白对K1 / K10和K3 / K12。在增生过程中，所有分层的鳞状上皮细胞都将K6 / K16角蛋白替换为基底上隔室中的这些角蛋白，从而排除了截短的分化。重要的是，经历伤口修复的体内角膜上皮的角蛋白模式模仿了培养的兔角膜上皮细胞的角蛋白模式。尽管培养的尿道上皮细胞继续合成尿道素，尿道素通常形成覆盖几乎整个顶端尿道上皮表面的二维结晶尿道素斑块，但这些蛋白质在培养细胞中并未组装成晶体。但是，培养的上皮细胞可在去除有丝分裂刺激，使用合适的细胞外基质或将细胞移植到体内非有丝分裂环境后迅速恢复正常分化。这些数据表明，培养的上皮细胞具有模仿体内再生或增生上皮的改变的分化模式。阻止组织特异性分化产物的合成，例如设计用于在角质化细胞中形成广泛的二硫键交联的K1和K10角蛋白，或uroplakin斑块的组装，可使上皮细胞更好地迁移和增殖，而这些活动至关重要在伤口修复过程中。培养的尿道上皮细胞和其他分层的上皮细胞为研究分化产物的合成和组装的调控提供了极好的模型，所述分化产物是上皮伤口修复过程中的关键细胞过程。

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