Kallen K J, Allan D, Whatmore J, Quinn P
Department of Physiology, University College London, UK.
Biochim Biophys Acta. 1994 Apr 20;1191(1):52-8. doi: 10.1016/0005-2736(94)90232-1.
Sphingomyelin, which has been degraded at the BHK cell surface by exogenous sphingomyelinase, is converted back into sphingomyelin with kinetics similar to those of plasma membrane recycling. Resynthesis of sphingomyelin under these conditions proceeds at a rate about 4-fold higher than normal biosynthesis of sphingomyelin. Neither resynthesis of sphingomyelin nor its return to the surface is inhibited by brefeldin A (BFA), which is a potent blocker of vesicular transport through the Golgi but has no effect on plasma membrane recycling. However, resynthesis of plasma membrane sphingomyelin is greatly decreased in cells undergoing mitosis or energy depletion, where endocytosis is inhibited. We conclude that the main site of surface sphingomyelin synthesis in BHK cells could be in recycling endosomes and not in the Golgi apparatus as proposed previously. We also suggest a model pathway by which cholesterol may reach the plasma membrane via recycling endosomes.
鞘磷脂在外源鞘磷脂酶作用下于BHK细胞表面降解后，会以与质膜循环相似的动力学重新转化为鞘磷脂。在这些条件下，鞘磷脂的重新合成速率比鞘磷脂的正常生物合成速率高约4倍。布雷菲德菌素A（BFA）对鞘磷脂的重新合成及其回到细胞表面均无抑制作用，BFA是一种通过高尔基体的囊泡运输的有效阻断剂，但对质膜循环没有影响。然而，在有丝分裂或能量耗竭的细胞中，质膜鞘磷脂的重新合成会大大减少，因为这些细胞的内吞作用受到抑制。我们得出结论，BHK细胞表面鞘磷脂合成的主要位点可能是在回收内体中，而不是如先前所认为的在高尔基体中。我们还提出了一个模型途径，胆固醇可能通过回收内体到达质膜。
