IL-1β Acts in Synergy with Endogenous IL-1β in A375-S2 Human Melanoma Cell Apoptosis Through Mitochondrial Pathway

Che, Wang; Wang, Minwei; Tashiro, Shin‐ichi; Onodera, Satoshi; Ikejima, Takashi

doi:10.3346/jkms.2005.20.4.555

Cited by 10 publications

(7 citation statements)

References 31 publications

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“…Thus, 100 µg/ml cis-UCA was optimally anti-inflammatory and cytoprotective against cellular damage caused by UV-B radiation in the present experimental setting. It should be noted that the decrease in mitochondrial metabolic activity measured by the MTT assay after UV-B irradiation may not be caused by the irradiation only because the UV-B dose induced IL-6 secretion at the nanomolar level, which can directly decrease MTT metabolism [30]. The UV-B irradiation induced caspase-3 activity in both cell types, which revealed apoptotic cell death and supported the MTT assay data.…”

Section: Discussionsupporting

confidence: 54%

Cis‐urocanic acid suppresses UV‐B‐induced interleukin‐6 secretion and cytotoxicity in human corneal and conjunctival epithelial cells in vitro

Viiri

Jauhonen

Ryhänen

et al. 2009

Acta Ophthalmologica

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PurposeUrocanic acid (UCA) is a major ultraviolet (UV)-absorbing endogenous chromophore in the epidermis and is also an efficacious immunosuppressant. The anti-inflammatory and cytoprotective effects of cis-UCA were studied in ocular surface cell cultures exposed to UV-B irradiation. MethodsHuman corneal epithelial cells (HCE-2) and human conjunctival epithelial cells (HCECs) were incubated with 10, 100, 1,000, and 5,000 μg/ml cis-UCA with and without a single UV-B irradiation dose. The concentrations of IL-1β, IL-6, IL-8, and TNF-α in the culture medium and caspase-3 activity in the cell extract sampled were measured by enzyme-linked immunosorbent assay (ELISA). Cell viability was measured by the colorimetric MTT (3-(4,5-dimethyldiazol- 2-yl)-2,5-diphenyltetrazolium bromide) assay. ResultsUV-B irradiation multiplied interleukin IL-6 and IL-8 secretion levels in HCE-2 cells and HCECs as analyzed with ELISA. Cell viability as measured by the MTT assay declined by 30%–50% in HCE-2 cells and by 20%–40% in HCECs after UV-B irradiation. Moreover, UV-B increased caspase-3 activity in both cell types as analyzed with ELISA. Treatment with 100 μg/ml cis-UCA completely suppressed IL-6 and IL-8 secretion, decreased caspase-3 activity, and improved cell viability against UV-B irradiation. No significant effects on IL-6 or IL-8 secretion, caspase-3 activity, or viability of the non-irradiated cells were observed with 100 μg/ml cis-UCA in both cell types. The 5,000 μg/ml concentration was toxic. ConclusionsThese findings indicate that cis-UCA may represent a promising anti-inflammatory and cytoprotective treatment option to suppress UV-B-induced inflammation and cellular damage in human corneal and conjunctival epithelial cells.

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Section: Discussionsupporting

confidence: 54%

Cis‐urocanic acid suppresses UV‐B‐induced interleukin‐6 secretion and cytotoxicity in human corneal and conjunctival epithelial cells in vitro

Viiri

Jauhonen

Ryhänen

et al. 2009

Acta Ophthalmologica

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“…IL-1β released from the activation of spinal microglia enhanced the AMPA response in neurons through IL-1R activation which led to acute and chronic pain, and IL-1R antagonist (IL-1RA) can abolish these effects of IL-1β (Gustafson-Vickers et al 2008;Kawasaki et al 2008;Liu et al 2013). IL-1β-induced apoptosis was mediated by mitochondria, through up-regulation of Bax and down-regulation of Bcl-2 and Bcl-x L to initiate caspase-9 activity, leading to the activation of caspase-3 in this apoptotic process (Wang et al 2005). IL-1R is expressed in the PC12 cells and IL-1β has toxic effect on PC12 cells by binding with IL-1R.…”

Section: Discussionmentioning

confidence: 99%

Activation of BV2 microglia by lipopolysaccharide triggers an inflammatory reaction in PC12 cell apoptosis through a toll-like receptor 4-dependent pathway

Dai

et al. 2015

Cell Stress and Chaperones

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Microglia play an important role in neuronal protection and damage. However, the molecular and cellular relationship between microglia and neurons is unclear. We carried out a prospective study to detect that activation of BV2 microglia induced PC12 cell apoptosis in vitro through the TLR4/adapter protein myeloid differentiation factor 88 (MyD88)/nuclear factor-κB (NF-κB) signaling pathway. BV2 microglia were treated with different concentrations of LPS for 24 h. Western blot was utilized to detect the expression of TLR4 and the downstream signaling pathway. The level of inflammatory mediator was quantified using a specific ELISA kit. The supernatant of 10 μg/ml LPS-treated BV2 cells was used as conditioned medium (CM). PC12 cells were co-culture with CM for 24 h. Cell viability was determined by MTT assay and cell apoptosis was tested by flow cytometry. BV2 microglia were treated with 10, 20, or 30 μg/ml LPS for 24 h. The expression of TLR4, MyD88, and NF-κB significantly increased. When PC12 cells were co-cultured with CM for 24 h, cell viability decreased. CM up-regulated the Bax level and down-regulated the Bcl-2 protein level in PC12 cells. PC12 cells pretreated with interleukin-1 receptor antagonist (IL-1RA) for 30 min, significantly alleviated CMinduced PC12 cell apoptosis. These results suggest that BV2 microglia activated by LPS triggered TLR4/MyD88/NF-κB signaling pathway that induced the release of IL-1β and could participate in the PC12 cells injury.

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“…In the study of Lui et al, this method was used for evaluating the inhibitory effects of a fusion protein of IL-1Ra with an extended half-life. The results showed that 32 nM of IL-1Ra led to 100 % inhibition effects of 1 ng/mL IL-1β [19]. The concentrations of IL-1Ra-ABD used in the present study were higher than those investigated by Lui et al In another study, Yu-Xin produced several mutated forms of IL-1Ra and compared their biological activities with those of native IL-1Ra.…”

Section: Discussionmentioning

confidence: 46%

“…For biological assay, on the other hand, we used the potent cytotoxic and apoptotic effects of IL-1β against cells with highly expressed of IL-1R [19]. Furthermore, based on the effects of Anakinra in preventing the cytotoxic effects of IL-1β, the protocol mentioned in the methods section was used.…”

Section: Discussionmentioning

confidence: 99%

Recombinant Production of IL-1Ra in Fusion to Albumin Binding Domain for Its Extended Half-Life

Shafiee

Yazdani

2021

Preprint

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Background: Anakinra, a FDA approved biological drug for Rheumatoid Arthritis, must be injected daily due to its short Half-life, leads to the lower patient compliance. So, the aim of this study was to produce IL-1Ra in fusing to albumin binding domain to extend its half-life and evaluate its biological effects.Methods and Results: The expression of IL-1Ra-ABD was performed in E. coli in fusing to intein1 of pTWIN1 in soluble and purified. The affinity of IL-1Ra-ABD to HSA was determined on Native-PAGE and its release percent toward time was determined. Finally, MTT assay was used to determine the antagonizing properties of recombinant IL-1Ra-ABD against IL-1β, on A375 cells. the expression induction of intein1-IL-1Ra-ABD using 0.1mM of IPTG at 15°C, and its cleavage represented a band approximately in 50 and 23 kDa respectively. Native-PAGE results showed that about 78% of IL-1Ra-ABD attached to the HSA after 2 hours of incubation, and MTT assay results showed no significant differences between the effects of our recombinant protein and native IL-1Ra.Conclusion: the production of soluble IL-1Ra-ABD with similar antagonizing effects to IL-1Ra was successfully performed. IL-1Ra-ABD showed suitable interaction with HSA and release over the time. However, pharmacokinetics and furthur biological evaluations are required.

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IL-1β Acts in Synergy with Endogenous IL-1β in A375-S2 Human Melanoma Cell Apoptosis Through Mitochondrial Pathway

Cited by 10 publications

References 31 publications

Cis‐urocanic acid suppresses UV‐B‐induced interleukin‐6 secretion and cytotoxicity in human corneal and conjunctival epithelial cells in vitro

Cis‐urocanic acid suppresses UV‐B‐induced interleukin‐6 secretion and cytotoxicity in human corneal and conjunctival epithelial cells in vitro

Activation of BV2 microglia by lipopolysaccharide triggers an inflammatory reaction in PC12 cell apoptosis through a toll-like receptor 4-dependent pathway

Recombinant Production of IL-1Ra in Fusion to Albumin Binding Domain for Its Extended Half-Life

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