Inhibition of NF-κB promotes autophagy via JNK signaling pathway in porcine granulosa cells

Gao, Hui; Lü, Lin; Haq, Ihtesham ul; Zeng, Shenming

doi:10.1016/j.bbrc.2016.03.101

Cited by 34 publications

(28 citation statements)

References 28 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In porcine primary granulosa cells, Gao et al . found that NF-κB activated autophagy via activation of the JNK pathway34. The JNK pathway might be associated with the up-regulation of autophagy in cancer cells.…”

Section: Discussionmentioning

confidence: 93%

Dihydroartemisinin inhibits catabolism in rat chondrocytes by activating autophagy via inhibition of the NF-κB pathway

Jiang

Meng

Lee

et al. 2016

Sci Rep

View full text Add to dashboard Cite

Osteoarthritis is a disease with inflammatory and catabolic imbalance in cartilage. Dihydroartemisinin (DHA), a natural and safe anti-malarial agent, has been reported to inhibit inflammation, but its effects on chondrocytes have yet to be elucidated. We investigated the effects of DHA on catabolism in chondrocytes. Viability of SD rats chondrocytes was analyzed. Autophagy levels were determined via expression of autophagic markers LC3 and ATG5, GFP-LC3 analysis, acridine orange staining, and electron microscopy. ATG5 siRNA induced autophagic inhibition. Catabolic gene and chemokine expression was evaluated using qPCR. The NF-κB inhibitor SM7368 and p65 over-expression were used to analyze the role of NF-κB pathway in autophagic activation. A concentration of 1 μM DHA without cytotoxicity increased LC3-II and ATG5 levels as well as autophagosomal numbers in chondrocytes. DHA inhibited TNF-α-induced expression of MMP-3 and -9, ADAMTS5, CCL-2 and -5, and CXCL1, which was reversed by autophagic inhibition. TNF-α-stimulated nuclear translocation and degradation of the p65 and IκBα proteins, respectively, were attenuated in DHA-treated chondrocytes. NF-κB inhibition activated autophagy in TNF-α-treated chondrocytes, but p65 over-expression reduced the autophagic response to DHA. These results indicate that DHA might suppress the levels of catabolic and inflammatory factors in chondrocytes by promoting autophagy via NF-κB pathway inhibition.

show abstract

Section: Discussionmentioning

confidence: 93%

Dihydroartemisinin inhibits catabolism in rat chondrocytes by activating autophagy via inhibition of the NF-κB pathway

Jiang

Meng

Lee

et al. 2016

Sci Rep

View full text Add to dashboard Cite

show abstract

“…Although granulosa cell (GC) apoptosis is confirmed to be the main reason for follicular atresia [2], increasing evidence suggests that autophagy is induced in ovarian GCs during follicular atresia to promote apoptotic cell death by excessive self-digestion and degradation of essential cellular constituents [3,4]. Autophagy is a potential mechanism to alleviate cellular stress induced by hyperthermia in different follicular stages of the pig ovary [5]; nevertheless, the inhibition of transcription factor nuclear factor-κB (NF-κB) increased autophagy of porcine granulosa cells via JNK signaling and promoted steroidogenesis [6].…”

Section: Introductionmentioning

confidence: 99%

Autophagy and Apoptosis of Porcine Ovarian Granulosa Cells During Follicular Development

Zheng

Liu

et al. 2019

Animals

View full text Add to dashboard Cite

Follicular atresia is closely related to both apoptosis and autophagy of granulosa cells (GCs) in ovarian follicles. In the present study, GCs were isolated from pig ovaries in small, medium and large antral follicles, and the current results showed that the proliferation of GCs was higher in medium follicles, and lower in large follicles compared to small follicles. The Bax and Caspase 3 mRNA levels were significantly higher, but the ratio of Bcl-2/Bax was lower in GCs of large follicles. The marker genes of autophagy, Atg3, Atg7 and LC3 mRNA levels were higher in GCs from medium follicles. Apoptosis- and autophagy-related proteins had a similar expression pattern to the mRNA level. Our results showed that phosphorylated ERK (p-ERK) was activated in GCs of large follicles, while phosphorylated AKT (p-AKT) and phosphorylated mTOR (p-mTOR) were inhibited in GCs of medium follicles. Labeling of autophagic vesicles with 4’,6-diamidino-2-phenylindole (DAPI) and monodansylcadaverine (MDC) confirmed the results of gene transcription and protein expression in GCs of different size follicles. We conclude that autophagy and apoptosis of GCs occurred in different size follicles during follicular development, and autophagy was mainly found in GCs of medium follicles, while apoptosis was mainly found in GCs of large follicles.

show abstract

“…The autophagy inhibitor chloroquine significantly inhibited bortezomib-induced IB␣ degradation, increased complex formation with NF-B, and reduced NF-B nuclear translocation and DNA binding activity in lymphoma cells (34). In addition, inhibition of NF-B promoted autophagy in porcine granulosa cells (35). AP-1 proteins such as junB and c-jun, but not junD or c-fos, have been shown to inhibit autophagy (36,37).…”

Section: Discussionmentioning

confidence: 98%

Bacteroides fragilis Enterotoxin Induces Formation of Autophagosomes in Endothelial Cells but Interferes with Fusion with Lysosomes for Complete Autophagic Flux through a Mitogen-Activated Protein Kinase-, AP-1-, and C/EBP Homologous Protein-Dependent Pathway

Jeon

Myung

et al. 2017

Infect Immun

View full text Add to dashboard Cite

Bacteroides fragilis enterotoxin (BFT), a virulence factor of enterotoxigenic B. fragilis (ETBF), plays an essential role in mucosal inflammation. Although autophagy contributes to the pathogenesis of diverse infectious diseases, little is known about autophagy in ETBF infection. This study was conducted to investigate the role of BFT in the autophagic process in endothelial cells (ECs). Stimulation of human umbilical vein ECs (HUVECs) with BFT increased light chain 3 protein II (LC3-II) conversion from LC3-I and protein expression of p62, Atg5, and Atg12. In addition, BFT-exposed ECs showed increased indices of autophagosomal fusion with lysosomes such as LC3-lysosome-associated protein 2 (LAMP2) colocalization and the percentage of red vesicles monitored by the expression of dual-tagged LC3B. BFT also upregulated expression of C/EBP homologous protein (CHOP), and inhibition of CHOP significantly increased indices of autophagosomal fusion with lysosomes. BFT activated an AP-1 transcription factor, in which suppression of AP-1 activity significantly downregulated CHOP and augmented autophagosomal fusion with lysosomes. Furthermore, suppression of Jun N-terminal protein kinase (JNK) mitogenactivated protein kinase (MAPK) significantly inhibited the AP-1 and CHOP signals, leading to an increase in autophagosomal fusion with lysosomes in BFT-stimulated ECs. These results suggest that BFT induced accumulation of autophagosomes in ECs, but activation of a signaling pathway involving JNK, AP-1, and CHOP may interfere with complete autophagy.KEYWORDS autophagy, Bacteroides fragilis enterotoxin, endothelial cells E nterotoxigenic Bacteroides fragilis (ETBF) is known to be associated with diarrheal diseases, inflammatory bowel diseases, and colorectal cancers. B. fragilis enterotoxin (BFT), a virulence factor of ETBF, is responsible for these diseases (1). Exposure to BFT results in the infiltration of inflammatory cells through endothelial cells (ECs) (2-4). Although aspects of pathogenesis regarding ETBF infection have been investigated, a more detailed understanding of the interaction between BFT and the host, especially BFT-induced changes in host cells, could reveal indispensable characteristics of ETBF infection.

show abstract

Inhibition of NF-κB promotes autophagy via JNK signaling pathway in porcine granulosa cells

Cited by 34 publications

References 28 publications

Dihydroartemisinin inhibits catabolism in rat chondrocytes by activating autophagy via inhibition of the NF-κB pathway

Dihydroartemisinin inhibits catabolism in rat chondrocytes by activating autophagy via inhibition of the NF-κB pathway

Autophagy and Apoptosis of Porcine Ovarian Granulosa Cells During Follicular Development

Bacteroides fragilis Enterotoxin Induces Formation of Autophagosomes in Endothelial Cells but Interferes with Fusion with Lysosomes for Complete Autophagic Flux through a Mitogen-Activated Protein Kinase-, AP-1-, and C/EBP Homologous Protein-Dependent Pathway

Contact Info

Product

Resources

About