Kanamori S, Waguri S, Shibata M, Isahara K, Ohsawa Y, Konishi A, Kametaka S, Watanabe T, Ebisu S, Kominami E, Uchiyama Y
Department of Conservative Dentistry, Osaka University Faculty of Dentistry, 1-8 Yamadaoka, Suita, Osaka, 565-0871, Japan.
Biochem Biophys Res Commun. 1998 Oct 9;251(1):204-8. doi: 10.1006/bbrc.1998.9416.
PC12 cells express well cation-independent mannose 6-phosphate receptors (CI-MPR), but not cation-dependent (CD)-MPR as much. To examine CD-MPR dependency of transport of cathepsins B and D to lysosomes in PC12 cells, we prepared the cells overexpressing CD-MPR. Immunoreactivity for cathepsin B became more distinct and larger in size in the transfected cells than in wild-type cells. No difference in the distribution of cathepsin D was seen between these two cells. The viability of the cells following serum deprivation was significantly higher in the transfected cells than in wild-type cells. This increased viability of the transfected cells was blocked by CA074, a specific inhibitor of cathepsin B, while pepstatin A suppressed the action of CA074. The results suggest that CD-MPR preferentially transport cathepsin B in PC12 cells, and cathepsins B and D participate in the regulation of PC12 cell apoptosis.
PC12细胞大量表达阳离子非依赖性甘露糖6-磷酸受体（CI-MPR），但阳离子依赖性（CD）-MPR的表达量则没那么多。为了检测PC12细胞中组织蛋白酶B和D向溶酶体转运对CD-MPR的依赖性，我们制备了过表达CD-MPR的细胞。与野生型细胞相比，转染细胞中组织蛋白酶B的免疫反应性在大小上变得更加明显且更大。这两种细胞之间组织蛋白酶D的分布没有差异。血清剥夺后，转染细胞的活力显著高于野生型细胞。组织蛋白酶B的特异性抑制剂CA074可阻断转染细胞这种增加的活力，而胃蛋白酶抑制剂A可抑制CA074的作用。结果表明，CD-MPR在PC12细胞中优先转运组织蛋白酶B，并且组织蛋白酶B和D参与PC12细胞凋亡的调控。
