Inhibition of NF-κB promotes autophagy via JNK signaling pathway in porcine granulosa cells
Inhibition of NF-κB promotes autophagy via JNK signaling pathway in porcine granulosa cells
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DOI：
10.1016/j.bbrc.2016.03.101
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发表时间：
2016
期刊：
影响因子：
--
通讯作者：
Shen-ming Zeng
中科院分区：
文献类型：
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作者：
Shen-ming Zeng
The transcription factor nuclear factor-kB (NF-kB) plays an important role in diverse processes, including cell proliferation and differentiation, apoptosis and inflammation. However, the role of NF-kB in porcine follicle development is not clearly elucidated. In this study, we demonstrated that follicle stimulating hormone (FSH) increased the level of inhibitor of NF-kB (IkB) protein and promoted the cytoplasmic localization of p65, indicating that FSH inhibits the activation of NF-kB in porcine granulosa cells. Moreover, inhibition of NF-kB by FSH or another specific inhibitor of NF-kB, pyrrolidine dithiocarbamate (PDTC), could activate JNK signaling and enhance autophagic activity in porcine granulosa cells. Knockdown of RelA (p65) Subunit of NF-kB by RNA interference abrogated the activation of JNK signaling pathway and the increase of autophagic protein expression by FSH. Meanwhile, the functional signi- ficance of FSH or PDTC-mediated autophagy were further investigated. Our results demonstrated that the increased autophagy promoted progesterone secretion in porcine granulosa cells. Blockage of autophagy by chloroquine obviated the FSH or PDTC-induced progesterone production. Taken together, these results indicate that inhibition of NF-kB increased autophagy via JNK signaling, and promote steroidogenesis in porcine granulosa cells. Our results provide new insights into the regulation and function of autophagy in mammalian follicle development.
