Depletion of serum-derived exosomes aggravates heat stress-induced damage of bovine mammary epithelial cells
Depletion of serum-derived exosomes aggravates heat stress-induced damage of bovine mammary epithelial cells
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DOI：
10.1007/s11033-022-07767-6
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发表时间：
2022-08
影响因子：
2.8
通讯作者：
Yue Wang;Huiling Wang;Zhiyuan Lin;Ji-feng Zhong;Kunlin Chen;Xing Duan
中科院分区：
文献类型：
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作者：
Yue Wang;Huiling Wang;Zhiyuan Lin;Ji-feng Zhong;Kunlin Chen;Xing Duan
研究背景外泌体参与细胞间通讯，影响多种生理和病理过程。本研究探讨了血清外泌体对热应激条件下牛乳腺上皮细胞（BMEC）功能和乳汁合成的影响。方法和结果我们用胎牛血清（FBS）或不含外泌体的FBS培养基培养BMEC，用CCK-8试剂盒检测其活力。结果表明，在无外泌体的培养基中培养细胞降低了活力并增加了活性氧的水平。在无外泌体的培养基中培养的BMEC具有降低的线粒体膜电位、降低的锰超氧化物歧化酶活性和破坏的线粒体动力学。他们表现出凋亡由于上调Drp 1，Fis 1，Bax和HSP 70。最后，我们观察到在无外泌体的培养基中培养细胞后，乳脂和乳蛋白相关基因：mTOR、PPARγ、p-mTOR和ADD 1以及SREBP 1、ELF 5和CSN 2分别下调。这些负面影响的exosome-free培养基上的BMEC可以进一步加强下heat stress.ConclusionOur结果表明，exosomes从血清是至关重要的，维持正常功能的BMEC。
BackgroundExosomes are involved in intercellular communication, affecting many physiological and pathological process. The present study evaluated the effects of serum exosomes on the function of bovine mammary epithelial cells (BMECs) and milk synthesis under heat stress.Methods and resultsWe cultured the BMECs in fetal bovine serum (FBS) or exosome-free FBS medium and examined, their viability using CCK-8 kit. The results showed that culturing the cells in an exosome-free medium decreased viability and increased the levels of reactive oxygen species. The BMECs cultured in the exosome-free medium had reduced mitochondrial membrane potential, decreased manganese superoxide dismutase activity, and disrupted mitochondrial dynamics. They exhibited apoptosis due to upregulated Drp1, Fis1, Bax and HSP70. Lastly, we observed downregulation of milk fat and lactoprotein-related genes: mTOR, PPARγ, p-mTOR and ADD1 and SREBP1, ELF5, and CSN2, respectively, after culturing the cells in an exosome-free medium. These negative effects of the exosome-free medium on the BMECs could be further reinforced under heat stress.ConclusionOur results demonstrated that exosomes from serum are critical for maintaining the normal function of BMECs.