Activation of RAW264.7 mouse macrophage cells in vitro through treatment with recombinant ricin toxin-binding subunit B: Involvement of protein tyrosine, NF-κB and JAK-STAT kinase signaling pathways

Xu, Na; Yuan, Hongyan; Liu, Wensen; Li, Songyan; Liu, Yang; Wan, Jiayu; Li, Xiaoyan; Zhang, Rui; Chang, Yaping

doi:10.3892/ijmm.2013.1426

Cited by 22 publications

(15 citation statements)

References 33 publications

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“…Relevant role of Akt in regulation of iNOS and COX-2 mRNA in STAT3KO macrophages was also elucidated using pharmacological inhibitors which are known to inhibit Akt activity in macrophages [ 57 , 88 , 89 ]. Treatment with BN82002 [ 57 ] and LY294002 [ 90 ] inhibited the mRNA expression of iNOS and COX-2 in STATKO cells stimulated with LPS for 1 h ( Figure 2 h). This result suggests that AKT together with Lyn and PI3K might be functionally involved in controlling gene expression of iNOS and COX-2 during STAT3 depletion conditions.…”

Section: Discussionmentioning

confidence: 99%

STAT3 Differentially Regulates TLR4-Mediated Inflammatory Responses in Early or Late Phases

Ahuja

Kim

Sung

et al. 2020

IJMS

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Toll-like receptor 4 (TLR4) signaling is an important therapeutic target to manage lipopolysaccharide (LPS)-induced inflammation. The transcription factor signal transducer and activator of transcription 3 (STAT3) has been identified as an important regulator of various immune-related diseases and has generated interest as a therapeutic target. Here, we investigated the time-dependent roles of STAT3 in LPS-stimulated RAW264.7 macrophages. STAT3 inhibition induced expression of the pro-inflammatory genes iNOS and COX-2 at early time points. STAT3 depletion resulted in regulation of nuclear translocation of nuclear factor (NF)-κB subunits p50 and p65 and IκBα/Akt/PI3K signaling. Moreover, we found that one Src family kinase, Lyn kinase, was phosphorylated in STAT3 knockout macrophages. In addition to using pharmacological inhibition of NF-κB, we found out that STAT3KO activation of NF-κB subunit p50 and p65 and expression of iNOS was significantly inhibited; furthermore, Akt tyrosine kinase inhibitors also inhibited iNOS and COX-2 gene expression during early time points of LPS stimulation, demonstrating an NF-κB- Akt-dependent mechanism. On the other hand, iNOS expression was downregulated after prolonged treatment with LPS. Activation of NF-κB signaling was also suppressed, and consequently, nitric oxide (NO) production and cell invasion were repressed. Overall, our data indicate that STAT3 differentially regulates early- and late-phase TLR4-mediated inflammatory responses.

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Section: Discussionmentioning

confidence: 99%

STAT3 Differentially Regulates TLR4-Mediated Inflammatory Responses in Early or Late Phases

Ahuja

Kim

Sung

et al. 2020

IJMS

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“…RT causes serious inflammation in animals as well as humans, thereby inducing the secretion of many cytokines by macrophages (Benson, Gomez, Wolf, Tibbetts, & March, 2011; Higuchi, Tamura, & Oda, 2003; Wong, Korcheva, Jacoby, & Magun, 2007b; Xu et al, 2013). Considering Retro‐2 could retain the capacity of protein synthesis inhibited by RT, the cytokine levels in the cell culture medium were determined to evaluate the effect of preprocessed Retro‐2 on levels of cytokines released by cells challenged with RT.…”

Section: Resultsmentioning

confidence: 99%

Pretreatment with Retro‐2 protects cells from death caused by ricin toxin by retaining the capacity of protein synthesis

Jiao

et al. 2020

J of Applied Toxicology

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The current study explores the detoxification effect of Retro‐2 on ricin toxin (RT) cytotoxicity, as well as the mechanisms underlying such effects, to provide a basis for follow‐up clinical applications of Retro‐2. The mouse‐derived mononuclear/macrophage cell line, RAW264.7, was used to evaluate the detoxification effect of Retro‐2 on RT by detecting cell viability, capacity for protein synthesis and the expression of cytokines, as well as endoplasmic reticulum stress (ERS)‐related mRNA. The results indicated that many cells died when challenged with concentrations of RT ≥50ng/mL. The protein synthesis capacity of cells decreased when challenged with 200ng/mL RT for 2hours. Furthermore, the synthesis and release of many cytokines decreased, while the expression of cytokines or ERS‐related mRNA increased when challenged with 200ng/mL of RT for 12 or more hours. However, cell viability, capacity for protein synthesis and release levels of many cytokines were higher, while the expression levels of cytokine, or ERS‐related mRNA, were lower in cells pretreated with 20μm Retro‐2 and challenged with RT, compared with those that had not been pretreated with Retro‐2. In conclusion, Retro‐2 retained the capacity for protein synthesis inhibited by RT, alleviated ERS induced by RT and increased the viability of cells challenged with RT. Retro‐2 shows the potential for clinical applications.

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“…Over-recruitment of immune cells leads to damaged normal cells. partly be due to modification of NF-κB signaling, which leads to expression of iNOS, cyclooxygenase COX , and proinflammatory cytokines, including TNF-α 14,26 . Oleic acid has been shown to abrogate NF-κB signaling in LPSstimulated RAW 264.7 cells 23 and β-AP-stimulated PC12 cells 24 .…”

Section: Discussionmentioning

confidence: 99%

Emu Oil Reduces LPS-Induced Production of Nitric Oxide and TNF-α but not Phagocytosis in RAW 264 Macrophages

Miyashita¹,

Minami

Ito

et al. 2018

J. Oleo Sci.

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Emu is the second-largest extant bird native to Australia. Emu oil, obtained from the emu's fat deposits, is used as an ingredient in cosmetic skincare products. Emu oil has been reported to improve several inflammatory symptoms; however, the mechanisms of these anti-inflammatory effects are largely unknown. This study investigated the effects of emu oil on the inflammatory macrophage response in vitro. A murine macrophage cell line, RAW 264, was incubated in culture media supplemented with or without emu oil and stimulated with lipopolysaccharide (LPS). We determined phagocytic activity by measuring the number of fluorescent microspheres taken up by the cells. The phagocytic activity of RAW 264 cells in the presence of LPS was unaffected by emu oil. We also determined production of nitric oxide (NO) and tumor necrosis factor (TNF)-α in the culture medium using the Griess reaction and an enzyme-linked immunosorbent assay, respectively, and the protein expression of inducible NO synthase (iNOS) using western blotting. The results indicated that emu oil reduced the LPS-induced production of NO, TNF-α, and iNOS expression in a dose-dependent manner. The results suggested that emu oil does not reduce the phagocytic clearance rate of inflammatory matter; however, it does reduce the production of NO and TNF-α in macrophages. These latter products enhance the inflammatory response and emu oil thereby demonstrated anti-inflammatory properties.

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Activation of RAW264.7 mouse macrophage cells in vitro through treatment with recombinant ricin toxin-binding subunit B: Involvement of protein tyrosine, NF-κB and JAK-STAT kinase signaling pathways

Cited by 22 publications

References 33 publications

STAT3 Differentially Regulates TLR4-Mediated Inflammatory Responses in Early or Late Phases

STAT3 Differentially Regulates TLR4-Mediated Inflammatory Responses in Early or Late Phases

Pretreatment with Retro‐2 protects cells from death caused by ricin toxin by retaining the capacity of protein synthesis

Emu Oil Reduces LPS-Induced Production of Nitric Oxide and TNF-α but not Phagocytosis in RAW 264 Macrophages

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