PDF(Pubmed)
Abstract：
UNASSIGNED: The skin barrier is the first line of defense of the body, while skin lipids play an important role in the skin permeability barrier. Lamellar bodies are also involved in maintaining the stability of the skin permeability barrier. However, the exact origin of lamellar bodies remains unclear. Recent studies have suggested that autophagy may participate in the formation of lamellar bodies.
UNASSIGNED: This study aimed to investigate the role of autophagy in the formation of lamellar bodies in keratinocytes and the regulation of keratinocyte lipids.
UNASSIGNED: Keratinocytes were incubated with autophagy inducer Rapamycin and autophagy inhibitor Bafilomycin A1. The changes in autophagy flux were detected by Western blot, and the formation of lamellar bodies was observed by transmission electron microscopy. Furthermore, the changes in keratinocytes lipidomics were detected by liquid chromatography-mass spectrometry.
UNASSIGNED: Our research showed that the autophagy inducer promoted autophagy activation and formation of lamellar bodies in keratinocytes, while the inhibitor inhibited autophagy signals and the formation of lamellar bodies in keratinocytes. In addition, the lipidomics results revealed a significant change in glycerophospholipids after autophagy induction and autophagy inhibition.
UNASSIGNED: These results demonstrate that autophagy may play an essential role in skin lipids via glycerophospholipids pathway.
UNASSIGNED: This study aimed to investigate the role of autophagy in the formation of lamellar bodies in keratinocytes and the regulation of keratinocyte lipids.
UNASSIGNED: Keratinocytes were incubated with autophagy inducer Rapamycin and autophagy inhibitor Bafilomycin A1. The changes in autophagy flux were detected by Western blot, and the formation of lamellar bodies was observed by transmission electron microscopy. Furthermore, the changes in keratinocytes lipidomics were detected by liquid chromatography-mass spectrometry.
UNASSIGNED: Our research showed that the autophagy inducer promoted autophagy activation and formation of lamellar bodies in keratinocytes, while the inhibitor inhibited autophagy signals and the formation of lamellar bodies in keratinocytes. In addition, the lipidomics results revealed a significant change in glycerophospholipids after autophagy induction and autophagy inhibition.
UNASSIGNED: These results demonstrate that autophagy may play an essential role in skin lipids via glycerophospholipids pathway.
摘要：
■皮肤屏障是身体的第一道防线，而皮肤脂质在皮肤渗透屏障中起着重要作用。层状体也参与维持皮肤渗透性屏障的稳定性。然而,层状体的确切起源尚不清楚。最近的研究表明，自噬可能参与了层状体的形成。
■本研究旨在研究自噬在角质形成细胞中层状体形成和角质形成细胞脂质调节中的作用。
■将角质形成细胞与自噬诱导剂雷帕霉素和自噬抑制剂巴弗洛霉素A1一起孵育。Westernblot检测自噬通量的变化,透射电镜观察到层状体的形成。此外，通过液相色谱-质谱法检测角质形成细胞脂质组学的变化。
■我们的研究表明，自噬诱导剂促进了角质形成细胞中自噬的激活和层状体的形成，该抑制剂抑制了角质形成细胞中的自噬信号和层状体的形成。此外,脂质组学结果显示，自噬诱导和自噬抑制后，甘油磷脂发生了显著变化。
■这些结果表明，自噬可能通过甘油磷脂途径在皮肤脂质中发挥重要作用。
■本研究旨在研究自噬在角质形成细胞中层状体形成和角质形成细胞脂质调节中的作用。
■将角质形成细胞与自噬诱导剂雷帕霉素和自噬抑制剂巴弗洛霉素A1一起孵育。Westernblot检测自噬通量的变化,透射电镜观察到层状体的形成。此外，通过液相色谱-质谱法检测角质形成细胞脂质组学的变化。
■我们的研究表明，自噬诱导剂促进了角质形成细胞中自噬的激活和层状体的形成，该抑制剂抑制了角质形成细胞中的自噬信号和层状体的形成。此外,脂质组学结果显示，自噬诱导和自噬抑制后，甘油磷脂发生了显著变化。
■这些结果表明，自噬可能通过甘油磷脂途径在皮肤脂质中发挥重要作用。
