Zhang Xiuguo, Tanaka Naoki, Nakajima Takero, Kamijo Yuji, Gonzalez Frank J, Aoyama Toshifumi
Department of Metabolic Regulation, Shinshu University Graduate School of Medicine, 3-1-1 Asahi, Matsumoto 390-8621, Japan.
Biochem Biophys Res Commun. 2006 Aug 11;346(4):1307-11. doi: 10.1016/j.bbrc.2006.06.042. Epub 2006 Jun 16.
Hepatic peroxisome proliferation, increases in the numerical and volume density of peroxisomes, is believed to be closely related to peroxisome proliferator-activated receptor alpha (PPARalpha) activation; however, it remains unknown whether peroxisome proliferation depends absolutely on this activation. To verify occurrence of PPARalpha-independent peroxisome proliferation, fenofibrate treatment was used, which was expected to significantly enhance PPARalpha dependence in the assay system. Surprisingly, a novel type of PPARalpha-independent peroxisome proliferation and enlargement was uncovered in PPARalpha-null mice. The increased expression of dynamin-like protein 1, but not peroxisome biogenesis factor 11alpha, might be associated with the PPARalpha-independent peroxisome proliferation at least in part.
肝脏过氧化物酶体增殖,即过氧化物酶体数量和体积密度的增加,被认为与过氧化物酶体增殖物激活受体α(PPARα)的激活密切相关;然而,过氧化物酶体增殖是否绝对依赖于这种激活仍不清楚。为了验证不依赖PPARα的过氧化物酶体增殖的发生情况,使用了非诺贝特处理,预期这会在检测系统中显著增强对PPARα的依赖性。令人惊讶的是,在PPARα基因敲除小鼠中发现了一种新型的不依赖PPARα的过氧化物酶体增殖和增大现象。动力蛋白样蛋白1的表达增加,而非过氧化物酶体生物发生因子11α的表达增加,可能至少部分地与不依赖PPARα的过氧化物酶体增殖有关。