A primary effect of palmitic acid on mouse oocytes is the disruption of the structure of the endoplasmic reticulum.

A primary effect of palmitic acid on mouse oocytes is the disruption of the structure of the endoplasmic reticulum.
复制标题

DOI:
10.1530/rep-21-0332
复制
发表时间:
2021-12-28
期刊:
Reproduction (Cambridge, England)
影响因子:
--
通讯作者:
Swann K
Swann K
中科院分区:
其他
文献类型:
--
作者:
Wang Y;Pope I;Brennan-Craddock H;Poole E;Langbein W;Borri P;Swann K

文献摘要

相似文献

小鼠卵母细胞暴露于棕榈酸 (PA) 等饱和脂肪酸 (FA) 中已被证明会增加脂质含量,并引起内质网 (ER) 应激反应和线粒体氧化还原状态的变化。 PA 还可以破坏其他细胞类型中的 Ca2+ 储存。这些细胞内变化之间的联系,或者它们是否被单不饱和脂肪酸(如油酸(OA))所阻止,尚不清楚。在这里,我们使用相干反斯托克斯拉曼散射和双光子荧光显微镜研究了 FA 对体外成熟的小鼠卵母细胞的影响。当卵母细胞在 PA 存在下成熟时,脂滴的聚集模式和大小会发生变化,而在 OA 中共孵育可以减轻这种变化。 PA 的单独成熟也会导致 ER 结构的明显破坏。通过将 OA 与 PA 一起孵育可以防止这种效应。相比之下,小鼠卵母细胞在含有 PA 的培养基中的成熟与线粒体氧化还原状态或细胞内储备的 Ca2+ 含量的任何显着变化无关。这些数据表明,饱和 FA(例如 PA)对卵母细胞的主要影响是破坏 ER 的结构,这并不是由于对线粒体或 Ca2+ 储存的影响。
Exposure of mouse oocytes to saturated fatty acids (FAs) such as palmitic acid (PA) has been shown to increase lipid content and cause an endoplasmic reticulum (ER) stress response and changes in the mitochondrial redox state. PA can also disrupt Ca2+ stores in other cell types. The links between these intracellular changes, or whether they are prevented by mono-unsaturated FAs such as oleic acid (OA), is unclear. Here, we have investigated the effects of FAs on mouse oocytes, that are maturated in vitro, using coherent anti-Stokes Raman scattering and two-photon fluorescence microscopy. When oocytes were matured in the presence of PA, there were changes in the aggregation pattern and size of lipid droplets that were mitigated by co-incubation in OA. Maturation in PA alone also caused a distinctive disruption of the ER structure. This effect was prevented by incubation of OA with PA. In contrast, maturation of mouse oocytes in medium containing PA was not associated with any significant change in the redox state of mitochondria or the Ca2+ content of intracellular stores. These data suggest that a primary effect of saturated FAs such as PA on oocytes is to disrupt the structure of the ER and this is not due to an effect on the mitochondria or Ca2+ stores.