The mitochondrial phospholipid (CL) has been linked to mitochondrial and cellular functions. It has been postulated that the composition of CL is of impact for mitochondrial energy metabolism and cell proliferation. Although a correlation between CL composition and proliferation could be demonstrated for several cell types, evidence for a causal relationship remains obscure. Here, we applied two independent approaches, i) supplementation of fatty acids and ii) knock-out of the phospholipid remodeling enzyme tafazzin, to manipulate CL composition and analyzed the response on proliferation of C6 glioma cells. Both strategies caused substantial changes in the distribution of cellular fatty acids as well as in the distribution of fatty acids incorporated in CL that were accompanied by changes of the composition of molecular CL species. These changes did not correlate with cell proliferation. However, knock-out of tafazzin caused dramatic reduction in proliferation of C6 glioma cells independent of CL composition. The mechanism of tafazzin-dependent restriction of proliferation remains unclear. Among the various fatty acids administered only palmitic acid restricted cell proliferation by induction of cell death.

中文翻译：

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C6胶质瘤细胞的增殖需要独立于心磷脂成分的磷脂重塑酶他法嗪。

线粒体磷脂（CL）已与线粒体和细胞功能相关。据推测，CL的组成对线粒体能量代谢和细胞增殖有影响。尽管可以证明几种细胞类型的CL组成与增殖之间存在相关性，但因果关系的证据仍然不清楚。在这里，我们应用了两种独立的方法，即i）补充脂肪酸和ii）敲除磷脂重​​塑酶他扎欣，以操纵CL的组成并分析对C6胶质瘤细胞增殖的反应。两种策略都引起细胞脂肪酸分布以及掺入CL的脂肪酸分布的实质性变化，并伴随着分子CL种类组成的变化。这些变化与细胞增殖无关。然而，敲除他法津引起的C6胶质瘤细胞增殖的大幅降低，与CL成分无关。他夫嗪依赖的增殖限制机制尚不清楚。在施用的各种脂肪酸中，仅棕榈酸通过诱导细胞死亡来限制细胞增殖。