Co-enzyme Q10 upregulates Hsp70 and protects chicken primary myocardial cells under in vitro heat stress via PKC/MAPK

Co-enzyme Q10 upregulates Hsp70 and protects chicken primary myocardial cells under in vitro heat stress via PKC/MAPK
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辅酶 Q10 上调 Hsp70,并通过 PKC/MAPK 保护体外热应激下的鸡原代心肌细胞。

DOI:
10.1007/s11010-018-3356-2
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发表时间:
2018-12-01
影响因子:
4.3
通讯作者:
Bao, Endong
Bao, Endong
中科院分区:
生物学3区
文献类型:
--
作者:
Xu, Jiao;Tang, Shu;Bao, Endong

文献摘要

被引文献

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本研究探讨了辅酶Q10对热应激鸡原代心肌细胞的保护作用机制。形态学观察表明,添加辅酶Q10可以保护心肌细胞免受热应激,减轻线粒体和细胞核的损伤,减少空泡线粒体的平均数量。我们之前已经证明辅酶Q10可以通过上调Hsp70的表达来保护心肌细胞。因此,我们对参与这一过程的信号通路进行了探索。除JNK1总表达外,各组总MAPK蛋白(P38MAPK、JNK、ERK)表达均未见变化。与仅热应激处理的HS组相比,辅酶Q10未能增加JNK1的表达。Q10的加入上调了p-P38MAPK、p-JNK和p-ERK1的表达。P38MAPK抑制剂和JNK抑制剂SB203580和SP600125分别减弱了辅酶Q10对Hsp70的上调,表明MAPK途径参与了辅酶Q10对Hsp70的上调。辅酶Q10上调热应激时p-MEK3/6和p-MEK4的表达,但不上调p-MEK7的表达。在热应激过程中,添加辅酶Q10后,p-PKC α和p-PKC β 1的表达也升高,添加PKC抑制剂可降低辅酶Q10诱导的Hsp70的表达。这证实PKC也与Hsp70的上调有关。在HS+Q10组中,添加SP600125或SB203580可增加热应激下细胞的凋亡。我们的研究结果表明,辅酶Q10在热应激过程中上调Hsp70的表达,通过PKC-MEK3/4/6-P38MAPK/JNK通路保护鸡原代心肌细胞。
In this report, we investigate the protective mechanism of co-enzyme Q10 on chicken primary myocardial cells during heat stress. Morphological observations indicate that addition of co-enzyme Q10 protects myocardial cells from heat stress, reduces the damage of mitochondria and nucleus, and decreases the mean number of vacuolated mitochondria. We have previously shown that co-enzyme Q10 can protect myocardial cells by upregulating the expression of Hsp70. Therefore, signaling pathways involved in this process were explored. No changes of total MAPK protein (P38MAPK, JNK, ERK) expression in the experimental groups were detected, with the exception of total JNK1. Co-enzyme Q10 failed to increase the expression of JNK1 compared to the HS group which was treated with heat stress only. Addition of Q10 upregulated the expression of p-P38MAPK, p-JNK, and p-ERK1. Inhibitors of P38MAPK and JNK, SB203580 and SP600125, respectively, weakened the upregulation of Hsp70 by co-enzyme Q10, indicating that MAPK pathways participate in the Hsp70 upregulation by co-enzyme Q10. Co-enzyme Q10 upregulates the expression of p-MEK3/6 and p-MEK4, but not p-MEK7 during heat stress. Expression of p-PKC alpha and p-PKC beta 1 was also elevated following the addition of co-enzyme Q10 during heat stress, and addition of PKC inhibitors decreased the expression of Hsp70 induced by co-enzyme Q10. This confirms that PKC is also associated with the upregulation of Hsp70. In HS+Q10 group, addition of SP600125 or SB203580 could increase cell apoptosis under heat stress. Our results suggest that co-enzyme Q10 upregulates the expression of Hsp70 during heat stress to protect chicken primary myocardial cells via the PKC-MEK3/4/6-P38MAPK/JNK pathways.