EA 3842 Homeostasie Cellulaire & Pathologies - Faculte de Medecine, Rue du Dr Marcland, Limoges Cedex, France R&D Department, SILAB, BP 213, Brive Cedex, France.
Exp Dermatol. 2011 Mar;20(3):263-8. doi: 10.1111/j.1600-0625.2010.01157.x. Epub 2010 Dec 17.
Studies have established that autophagy constitutes an efficient process to recycle cellular components and certain proteins. The phenomenon was demonstrated primarily in response to nutrient starvation, and there are increasing evidences that it is implied in differentiation. Keratinocyte differentiation was going along an activation of lysosomal enzymes and organelle clearance, and terminal steps are sometimes described as a specialized form of cell death leading to corneocytes. We examined whether initiation of the process in human keratinocyte HaCaT involves autophagy. The KSFM™ culture medium was substituted by M199, which contains a low glucose concentration but a high calcium level (known to induce differentiation). Metabolic stress reduced enhanced cell number in G(1) phase, without apoptotic features (ΔΨmt and membrane integrity are unchanged). Morphological changes were associated with a lower integrin ß1 expression and modifications of protein levels involved in keratinocyte differentiation (involucrin, keratin K10 and ΔNp63α). Whereas autophagic signalling was supported by SIRT1 and pAMPK (T172) increase according to time kinetic, which led to the disappearance of mTOR phosphorylated on S2448 residue. The significant Bcl-X(L) level reduction with stress promoted autophagy, by the release of Beclin-1, whereas ATG5-ATG12 and LC3-II that are involved in autophagosome formation were enhanced significantly. Then, the level of lysosomal protein cathepsin B rose to execute autophagy. Kinetic studies established that autophagy would constitute an early signalling process required for keratinocyte commitment in differentiation pathway.
研究已经证实,自噬是细胞成分和某些蛋白质再循环的有效过程。这种现象主要是在营养饥饿时表现出来的,而且越来越多的证据表明它与分化有关。角质形成细胞分化伴随着溶酶体酶和细胞器的清除,终末步骤有时被描述为一种特殊形式的细胞死亡,导致角质细胞。我们研究了人角质形成细胞 HaCaT 中该过程的启动是否涉及自噬。用 M199 替代 KSFM™培养基,M199 含有低葡萄糖浓度但高钙水平(已知诱导分化)。代谢应激减少了 G1 期增强的细胞数量,但没有凋亡特征(ΔΨmt 和膜完整性不变)。形态变化与整合素β1表达降低以及与角质形成细胞分化相关的蛋白水平变化(包裹蛋白、角蛋白 K10 和 ΔNp63α)有关。自噬信号由 SIRT1 和 pAMPK(T172)增加支持,根据时间动力学,这导致 mTOR 在 S2448 残基上的磷酸化消失。应激时 Bcl-X(L)水平的显著降低促进了自噬,通过 Beclin-1 的释放,而 ATG5-ATG12 和 LC3-II 的形成则显著增强。然后,溶酶体蛋白组织蛋白酶 B 的水平上升以执行自噬。动力学研究表明,自噬将构成角质形成细胞在分化途径中分化承诺的早期信号过程。