Endoplasmic reticulum stress is involved in lipid accumulation induced by oleic acid in adipocytes of grass carp (Ctenopharyngodon idella): focusing on the transcriptional level
Endoplasmic reticulum stress is involved in lipid accumulation induced by oleic acid in adipocytes of grass carp (Ctenopharyngodon idella): focusing on the transcriptional level
复制标题
内质网应激参与草鱼（Ctenopharyngodon idella）脂肪细胞中油酸诱导的脂质积累：重点关注转录水平。
DOI：
10.1007/s10695-021-01031-7
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发表时间：
2022-01-29
影响因子：
2.9
通讯作者：
Ji, Hong
中科院分区：
文献类型：
--
作者：
Bian, Chenchen;Sun, Jian;Ji, Hong
人们普遍认为内质网应激（ER应激）与哺乳动物的脂质积累有关，但对鱼类的内质网应激知之甚少。本研究旨在从转录水平上阐明内质网应激在单不饱和油酸（OA）诱导的脂质积累中的作用。分别用200 μ M和400 μ M OA处理草鱼脂肪细胞，对照组用2%牛血清白蛋白（BSA）处理。结果表明，400 μ moa处理显著提高了细胞活力，同时刺激内质网应激更明显地促进了中性脂质积累。虽然脂解和脂肪酸氧化同时被激活，但OA的主要作用似乎是促进脂质积累。为了进一步探讨内质网应激是否影响脂质积累，我们使用有效的内质网应激抑制剂4-苯基丁酸（4- pba）对细胞进行预处理4小时。不出意料，我们发现内质网应激相关基因mRNA表达量下降。细胞内甘油三酯（TG）含量也降低，这与成脂因子和成脂转录因子及其靶基因的mRNA表达一致。总的来说，我们的数据表明内质网应激可能通过激活脂肪生成和脂肪生成参与了oa诱导的脂肪细胞脂质积累。基于此，可以采用保护内质网的策略来缓解草鱼脂肪组织中脂肪的过度积累。
It has been extensively claimed that endoplasmic reticulum stress (ER stress) is related to lipid accumulation in mammals, but little is known in fish. This study aims at elucidating the role of ER stress in mediating lipid accumulation induced by monounsaturated oleic acid (OA) with a focus on the transcriptional level. We treated the adipocytes of grass carp with 200 mu M and 400 mu M OA, respectively, while the control group was treated with 2% bovine serum albumin (BSA). The results showed that cell viability was significantly improved, while 400 mu M OA treatment promoted neutral lipid accumulation along with stimulating ER stress more obviously. Although lipolysis and fatty acid beta-oxidation were activated simultaneously, the primary effect of OA seems to be promotion of lipid accumulation. To further explore whether ER stress affects lipid accumulation, 4-phenyl butyric acid (4-PBA), an effective inhibitor of ER stress, was used to pretreat the cells for 4 h. Unsurprisingly, it was found that the mRNA expressions of genes linked with ER stress were decreased. Intracellular triglyceride (TG) content was also decreased, which was in accordance with the mRNA expressions of adipogenic and lipogenic transcription factors as well as their target genes. Collectively, our data shows that ER stress may take part in OA-induced lipid accumulation in adipocytes via activating adipogenesis and lipogenesis. Based on this, strategies for protecting ER could be used to alleviate excessive accumulation of lipid in grass carp adipose tissue.