Lang D M, Hille M G, Schwab M E, Stuermer C A
Faculty of Biology, University of Konstanz, Germany.
J Neurosci. 1996 Sep 15;16(18):5741-8. doi: 10.1523/JNEUROSCI.16-18-05741.1996.
Although growth cones typically collapse after encountering O1/galactocerebroside (GalC)-positive oligodendrocytes, the majority of growth cones traversed oligodendrocytes, which were raised for 8-10 d in medium containing 10 ng/ml platelet-derived growth factor (PDGF). Oligodendrocytes raised 8-10 d in control medium caused growth cone collapse as they normally do, but failed to elicit this response after being transferred to PDGF-containing medium for an additional 8-10 d. The opposite was observed when PDGF-treated oligodendrocytes were brought to control medium. Growth cones collapsed when contacting these cells. Oligodendrocytes also lost their collapse-inducing activity when raised in medium conditioned by astrocytes, known to produce PDGF. Antibody IN-1 is directed against against neurite growth inhibitors (NI), proteins of 35 and 250 kDa on the surface of O1/GalC-positive oligodendrocytes, which are known to elicit growth cone collapse. IN-1 immunoreactivity was markedly reduced in PDGF-treated oligodendrocytes. However, both PDGF-treated and control oligodendrocytes exhibited myelin-associated glycoprotein, proteolipid protein, and myelin basic protein immunoreactivity. This suggests that PDGF-treatment affects NI expression but does not interfere with the expression of advanced myelin marker proteins. Because NI cause growth cone collapse, the loss of collapse-inducing activity by PDGF-treated oligodendrocytes suggests that PDGF regulates, directly or indirectly, the expression of these proteins.
尽管生长锥在遇到O1/半乳糖脑苷脂(GalC)阳性少突胶质细胞后通常会塌陷,但大多数生长锥穿过了少突胶质细胞,这些少突胶质细胞在含有10 ng/ml血小板衍生生长因子(PDGF)的培养基中培养了8 - 10天。在对照培养基中培养8 - 10天的少突胶质细胞如正常情况一样会导致生长锥塌陷,但在转移到含PDGF的培养基中再培养8 - 10天后就无法引发这种反应。当将经PDGF处理的少突胶质细胞转移到对照培养基中时,观察到相反的情况。生长锥与这些细胞接触时会塌陷。当在已知能产生PDGF的星形胶质细胞条件培养基中培养时,少突胶质细胞也会失去其塌陷诱导活性。抗体IN-1针对的是神经突生长抑制剂(NI),即O1/GalC阳性少突胶质细胞表面的35 kDa和250 kDa蛋白质,已知它们会引发生长锥塌陷。在经PDGF处理的少突胶质细胞中,IN-1免疫反应性明显降低。然而,经PDGF处理的少突胶质细胞和对照少突胶质细胞均表现出髓鞘相关糖蛋白、蛋白脂蛋白和髓鞘碱性蛋白免疫反应性。这表明PDGF处理会影响NI的表达,但不会干扰晚期髓鞘标记蛋白的表达。由于NI会导致生长锥塌陷,经PDGF处理的少突胶质细胞失去塌陷诱导活性表明PDGF直接或间接调节这些蛋白质的表达。