Onset of re-epithelialization after skin injury correlates with a reorganization of keratin filaments in wound edge keratinocytes: defining a potential role for keratin 16.
Onset of re-epithelialization after skin injury correlates with a reorganization of keratin filaments in wound edge keratinocytes: defining a potential role for keratin 16.
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DOI：
10.1083/jcb.132.3.381
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发表时间：
1996-02
期刊：
影响因子：
--
通讯作者：
Coulombe PA
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文献类型：
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作者：
Paladini RD;Takahashi K;Bravo NS;Coulombe PA
复层上皮损伤会导致位于伤口边缘的有丝分裂后角质形成细胞中强烈诱导角蛋白 6 (K6) 和 16 (K16)。我们发现 K6 和 K16 的诱导发生在人表皮损伤后 6 小时内。它们随后在角质形成细胞中的积累与角蛋白丝的深刻重组相关，从泛细胞质分布到丝聚集在核旁位置，与细胞迁移的方向相反。这种细丝重组与额外的细胞结构变化以及损伤后 18 小时后上皮细胞再生的开始同时发生。通过跟踪 K6 和 K16 在体外和培养细胞中的组装，我们发现，相对于在表皮中组成性表达的特征明确的角蛋白对 K5 和 K14，K6 和 K16 聚合成 10 nm 短丝，在细胞核附近聚集，这是 K16 产生的特性。在转基因小鼠的皮肤角质形成细胞中强制表达人 K16 会导致角蛋白丝从细胞外围缩回，通常以极化方式缩回。这些结果表明 K16 可能不具有类似于表皮角蛋白的主要结构功能。相反，他们认为，在表皮伤口愈合的背景下，K16 的功能可能是促进角蛋白丝细胞质阵列的重组，这是角质形成细胞开始迁移到伤口部位之前的事件。
Injury to stratified epithelia causes a strong induction of keratins 6 (K6) and 16 (K16) in post-mitotic keratinocytes located at the wound edge. We show that induction of K6 and K16 occurs within 6 h after injury to human epidermis. Their subsequent accumulation in keratinocytes correlates with the profound reorganization of keratin filaments from a pan-cytoplasmic distribution to one in which filaments are aggregated in a juxtanuclear location, opposite to the direction of cell migration. This filament reorganization coincides with additional cytoarchitectural changes and the onset of re-epithelialization after 18 h post-injury. By following the assembly of K6 and K16 in vitro and in cultured cells, we find that relative to K5 and K14, a well- characterized keratin pair that is constitutively expressed in epidermis, K6 and K16 polymerize into short 10-nm filaments that accumulate near the nucleus, a property arising from K16. Forced expression of human K16 in skin keratinocytes of transgenic mice causes a retraction of keratin filaments from the cell periphery, often in a polarized fashion. These results imply that K16 may not have a primary structural function akin to epidermal keratins. Rather, they suggest that in the context of epidermal wound healing, the function of K16 could be to promote a reorganization of the cytoplasmic array of keratin filaments, an event that precedes the onset of keratinocyte migration into the wound site.