The lipid droplet coat protein perilipin 5 also localizes to muscle mitochondria.

The lipid droplet coat protein perilipin 5 also localizes to muscle mitochondria.
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脂滴外壳蛋白 perilipin 5 也定位于肌肉线粒体。

DOI:
10.1007/s00418-011-0888-x
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发表时间:
2012-02
影响因子:
2.3
通讯作者:
Hesselink, Matthijs K. C.
Hesselink, Matthijs K. C.
中科院分区:
生物学3区
文献类型:
--
作者:
Bosma, Madeleen;Minnaard, Ronnie;Sparks, Lauren M.;Schaart, Gert;Losen, Mario;de Baets, Marc H.;Duimel, Hans;Kersten, Sander;Bickel, Perry E.;Schrauwen, Patrick;Hesselink, Matthijs K. C.

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周脂蛋白5(PLIN 5/OXPAT)是主要存在于具有高脂肪氧化能力的组织中的脂滴(LD)外壳蛋白,表明PLIN 5在促进脂肪酸氧化中的作用。在这里,我们研究了PLIN 5在骨骼肌脂肪氧化中的作用。在人骨骼肌中,我们观察到PLIN 5(而不是PLIN 2)蛋白含量与OXPHOS含量紧密相关,并且在大鼠肌肉中PLIN 5含量与脂质衍生底物上的线粒体呼吸速率相关。这促使我们在分离的线粒体中通过免疫金电子显微镜和蛋白质印迹检测骨骼肌线粒体中PLIN 5蛋白的表达。这些数据表明,与PLIN 2相反,PLIN 5不仅定位于LD,而且定位于线粒体,可能促进脂肪酸氧化。大鼠胫骨前肌中PLIN 5的单侧过表达增强了肌细胞脂肪储存,而不增加线粒体密度,如OXPHOS系统的五种组分的蛋白质含量缺乏变化所示。从PLIN 5过表达的肌肉中分离的线粒体不具有增加的脂肪酸呼吸。然而有趣的是,在来自PLIN 5过表达肌肉的肌肉匀浆中的14 C-棕榈酸氧化测定显示完全脂肪酸氧化增加44.8%(P = 0.05)。因此,在缺乏LD的线粒体分离物中,PLIN 5不增加脂肪氧化,而在含有PLIN 5包被的LD的匀浆中,PLIN 5过表达时脂肪氧化更高。PLIN 5在线粒体中的存在有助于理解为什么PLIN 5与PLIN 2相反,在脂肪氧化组织中具有特殊的重要性。我们的数据表明PLIN 5参与将脂肪酸从LD引导至线粒体脂肪酸氧化。
Perilipin 5 (PLIN5/OXPAT) is a lipid droplet (LD) coat protein mainly present in tissues with a high fat-oxidative capacity, suggesting a role for PLIN5 in facilitating fatty acid oxidation. Here, we investigated the role of PLIN5 in fat oxidation in skeletal muscle. In human skeletal muscle, we observed that PLIN5 (but not PLIN2) protein content correlated tightly with OXPHOS content and in rat muscle PLIN5 content correlated with mitochondrial respiration rates on a lipid-derived substrate. This prompted us to examine PLIN5 protein expression in skeletal muscle mitochondria by means of immunogold electron microscopy and Western blots in isolated mitochondria. These data show that PLIN5, in contrast to PLIN2, not only localizes to LD but also to mitochondria, possibly facilitating fatty acid oxidation. Unilateral overexpression of PLIN5 in rat anterior tibialis muscle augmented myocellular fat storage without increasing mitochondrial density as indicated by the lack of change in protein content of five components of the OXPHOS system. Mitochondria isolated from PLIN5 overexpressing muscles did not possess increased fatty acid respiration. Interestingly though, 14C-palmitate oxidation assays in muscle homogenates from PLIN5 overexpressing muscles revealed a 44.8% (P = 0.05) increase in complete fatty acid oxidation. Thus, in mitochondrial isolations devoid of LD, PLIN5 does not augment fat oxidation, while in homogenates containing PLIN5-coated LD, fat oxidation is higher upon PLIN5 overexpression. The presence of PLIN5 in mitochondria helps to understand why PLIN5, in contrast to PLIN2, is of specific importance in fat oxidative tissues. Our data suggests involvement of PLIN5 in directing fatty acids from the LD to mitochondrial fatty acid oxidation.
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