2,3′,4,4′,5-Pentachlorobiphenyl Induces Inflammatory Responses in the Thyroid Through JNK and Aryl Hydrocarbon Receptor-Mediated Pathway

Xu, Bojin; Yang, Hui; Sun, Minne; Chen, Huanhuan; Jiang, Lin; Zheng, Xuqin; Ding, Guoxian; Liu, Yun; Sheng, Yunlu; Cui, Dai; Duan, Yu

doi:10.1093/toxsci/kfv235

Cited by 24 publications

(13 citation statements)

References 52 publications

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“…Indeed, previous studies using the FRTL-5 cells have demonstrated that quercetin has anti-thyroid effects inhibiting the expression of the thyroid-specific genes NIS, TSHR, TPO and TG [10,11]. At least some of these effects may be mediated by AP-1 activation, as suggested by the observation that jun activation is associated with a decrease of NIS gene expression [48]. Of course, more detailed studies are needed to know which factors of the AP-1 family are activated by quercetin in thyroid cells and how they interact with the regulatory regions of the genes involved.…”

Section: Discussionmentioning

confidence: 99%

The Flavonoid Quercetin Induces AP-1 Activation in FRTL-5 Thyroid Cells

Giuliani

2019

Antioxidants

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Previous studies have shown that quercetin inhibits thyroid function both in vitro and in vivo. An attempt to evaluate the effect of quercetin at the promoter level of the thyroid-specific genes led to the observation that this compound induces the basal activity of the reporter vector. Therefore, the action of quercetin has been evaluated on the basal activity of several reporter vectors: The PGL3 basic, promoter and control vectors from Promega, and a pSV-based chloramphenicol acetyltransferase (CAT) reporter vector. In the Fisher Rat Thyroid cell Line FRTL-5 thyroid cells transiently transfected, quercetin 10 μM increased the basal activity of all the reporter vectors evaluated, although the degree of the effect was significantly different among them. The analysis of the difference among the regulatory regions of these vectors identified the activator protein 1 (AP-1) binding site as one of the potential sites involved in the quercetin effect. Electromobility shift assay experiments showed that the treatment with quercetin induced the binding of a protein complex to an oligonucleotide containing the AP-1 consensus binding site. This is the first study showing an effect of quercetin on AP-1 activity in thyroid cells. Further studies are in progress to understand the role of AP-1 activation in the effects of quercetin on thyroid function.

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Section: Discussionmentioning

confidence: 99%

The Flavonoid Quercetin Induces AP-1 Activation in FRTL-5 Thyroid Cells

Giuliani

2019

Antioxidants

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“…Calibrations always gave an R 2 above 0.96 and allowed the quantification of SP and IBs. This method has been used in over 700 publications to date and is known to give precise data (e.g., Matusica et al 2016 ; Wahlang et al 2016 ; Xu et al 2016 ).…”

Section: Methodsmentioning

confidence: 99%

The E. coli pET expression system revisited—mechanistic correlation between glucose and lactose uptake

Wurm

Veiter

Ulonska

et al. 2016

Appl Microbiol Biotechnol

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Therapeutic monoclonal antibodies are mainly produced in mammalian cells to date. However, unglycosylated antibody fragments can also be produced in the bacterium Escherichia coli which brings several advantages, like growth on cheap media and high productivity. One of the most popular E. coli strains for recombinant protein production is E. coli BL21(DE3) which is usually used in combination with the pET expression system. However, it is well known that induction by isopropyl β-d-1-thiogalactopyranoside (IPTG) stresses the cells and can lead to the formation of insoluble inclusion bodies. In this study, we revisited the pET expression system for the production of a novel antibody single-chain variable fragment (scFv) with the goal of maximizing the amount of soluble product. Thus, we (1) investigated whether lactose favors the recombinant production of soluble scFv compared to IPTG, (2) investigated whether the formation of soluble product can be influenced by the specific glucose uptake rate (qs,glu) during lactose induction, and (3) determined the mechanistic correlation between the specific lactose uptake rate (qs,lac) and qs,glu. We found that lactose induction gave a much greater amount of soluble scFv compared to IPTG, even when the growth rate was increased. Furthermore, we showed that the production of soluble protein could be tuned by varying qs,glu during lactose induction. Finally, we established a simple model describing the mechanistic correlation between qs,lac and qs,glu allowing tailored feeding and prevention of sugar accumulation. We believe that this mechanistic model might serve as platform knowledge for E. coli.Electronic supplementary materialThe online version of this article (doi:10.1007/s00253-016-7620-7) contains supplementary material, which is available to authorized users.

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“…Additionally, as a highly conserved pathway, the c-Jun N-terminal kinase (JNK) signaling pathway functions crucially in regulating gene expression and intracellular metabolism in life activities, including growth and development, apoptosis and cellular response to external stress (20). Recently, the activation of the JNK signaling pathway was reported to mediate thyroid dysfunction re sulting from thyroid inflammatory responses and polychlorinated biphenyls (21). Based on existing knowledge, gene expression microarray analysis was performed to screen differentially expressed genes (DEGs) associated with TC and determine an unclarified gene, LRRK2, associated with TC.…”

Section: Introductionmentioning

confidence: 99%

Downregulated LRRK2 gene expression inhibits proliferation and migration while promoting the apoptosis of thyroid cancer cells by inhibiting activation of the JNK signaling pathway

et al. 2019

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Emerging studies have indicated that leucine-rich repeat kinase 2 (LRRK2) is associated with thyroid cancer (TC). The present study investigated the effect of LRRK2 on the cell cycle and apoptosis in TC, and examined the underlying mechanisms in vitro . To screen TC-associated differentially expressed genes, gene expression microarray analysis was conducted. Retrieval of pathways associated with TC from the Kyoto Encyclopedia of Genes and Genomes database indicated that the c-Jun N-terminal kinase (JNK) signaling pathway serves an essential role in TC. SW579, IHH-4, TFC-133, TPC-1 and Nthy-ori3-1 cell lines were used to screen cell lines with the highest and lowest LRRK2 expression for subsequent experiments. The two selected cell lines were transfected with pcDNA-LRRK2, or small interfering RNA against LRRK2 or SP600125 (a JNK inhibitor). Subsequently, flow cytometry, terminal deoxynucleotidyl transferase-mediated dUTP-biotin nick end labeling, a 5-ethynyl-2′-deoxyuridine assay and a scratch test was conducted to detect the cell cycle distribution, apoptosis, proliferation and migration, respectively, in each group. The LRRK2 gene was determined to be elevated in TC based on the microarray data of the GSE3678 dataset. The SW579 cell line was identified to exhibit the highest LRRK2 expression, while IHH-4 cells exhibited the lowest LRRK2 expression. LRRK2 silencing, through inhibiting the activation of the JNK signaling pathway, increased the expression levels of genes and proteins associated with cell cycle arrest and apoptosis in TC cells, promoted cell cycle arrest and apoptosis, and inhibited cell migration and proliferation in TC cells, indicating that LRRK2 repression could exert beneficial effects through the JNK signaling pathway on TC cells. These observations demonstrate that LRRK2 silencing promotes TC cell growth inhibition, and facilitates apoptosis and cell cycle arrest. The JNK signaling pathway may serve a crucial role in mediating the anti-carcinogenic activities of downregulated LRRK2 in TC.

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2,3′,4,4′,5-Pentachlorobiphenyl Induces Inflammatory Responses in the Thyroid Through JNK and Aryl Hydrocarbon Receptor-Mediated Pathway

Cited by 24 publications

References 52 publications

The Flavonoid Quercetin Induces AP-1 Activation in FRTL-5 Thyroid Cells

The Flavonoid Quercetin Induces AP-1 Activation in FRTL-5 Thyroid Cells

The E. coli pET expression system revisited—mechanistic correlation between glucose and lactose uptake

Downregulated LRRK2 gene expression inhibits proliferation and migration while promoting the apoptosis of thyroid cancer cells by inhibiting activation of the JNK signaling pathway

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