Interferon (IFN)-induced protein 35 (IFI35) negatively regulates IFN-β-phosphorylated STAT1-RIG-I-CXCL10/CCL5 axis in U373MG astrocytoma cells treated with polyinosinic-polycytidylic acid

Shirai, Kyogo; Shimada, Tatsuya; Yoshida, Hidemi; Hayakari, Ryo; Matsumiya, Tomoh; Tanji, Kunikazu; Murakami, Manabu; Tanaka, Hiroshi; Imaizumi, Tadaatsu

doi:10.1016/j.brainres.2017.01.018

Cited by 21 publications

(18 citation statements)

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“…3), and we used the 30-μg/mL dose of poly IC in the following experiments. astrocytoma cells (22) and in human mesangial cells (6), although findings have suggested that the poly IC-induced TLR3-NF-κB/IRF3-CCL5 pathway is active in a case of human biliary epithelial cells (21). In this study, we confirmed that the poly IC-induced TLR3-IFN-β-pSTAT1-RIG-I pathway involved in upstream of CCL2/5 production is active not only in astrocytoma cells but also in neuroblastoma cells.…”

Section: Time-and Concentration-dependent Poly Ic-induced Mrna Expressupporting

confidence: 75%

“…89081403) and human neuroblastoma SH-SY5Y cells (ECACC No. 94030304) were purchased from the European Collection of Authenticated Cell Cultures (Porton Down, UK) and cultured in DMEM (for U373MG) and DMEM/F12 (for SH-SY5Y) containing GlutaMAX™-I supplemented with 10% FBS (22,32). U373MG and SH-SY5Y cells have properties of astrocytes (7) and catecholaminergic neurons (30), respectively.…”

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confidence: 99%

“…We have previously found that human astrocytoma U373MG cells, used as a model of astrocytes, release CCL5 following the induction of RIG-I when treated with poly IC (31). We also reported that poly IC activates TLR3 signaling in U373MG cells (8) and that the TLR3-interferon (IFN)-β-phosphorylated STAT1 (signal transducer and activator of transcription protein 1)-RIG-I signaling pathway mediates the poly IC-induced CCL5 expression (6,22). Gnetin C is one of the resveratrol dimers (16) and is known to have cytoprotective functions (4), including radical scavenging activity, similar to that of ascorbic acid and dl-α-tocopherol (11).…”

mentioning

confidence: 99%

“…Gnetin C is one of the resveratrol dimers (16) and is known to have cytoprotective functions (4), including radical scavenging activity, similar to that of ascorbic acid and dl-α-tocopherol (11). We recently found that gnetin C decreases neurotoxic amyloid-β (Aβ) production and ameliorates Aβ-induced neurotoxicity in cultured human neuroblastoma cells (22). However, the effect of gnetin C on inflammatory signaling pathways leading to chemokine production has not been reported.…”

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confidence: 99%

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Gnetin C suppresses double-stranded RNA-induced C-C motif chemokine ligand 2 (CCL2) and CCL5 production by inhibiting Toll-like receptor 3 signaling pathway

et al. 2018

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The innate immune system is a prerequisite for biophylactic ability, but its dysregulation can cause inflammatory and autoimmune diseases. To determine a safe method of controlling inflammatory reactions in the brain, we examined the effects of gnetin C, a natural resveratrol dimer, on CC motif chemokine ligand 2 (CCL2) and CCL5 (pro-inflammatory chemokines) production observed after treatment with polyinosinic-polycytidylic acid [poly IC; a synthetic analog of dsRNA as a Toll-like receptor 3 (TRL3) ligand, 30 μg/mL] in cultured human astrocytoma U373MG and neuroblastoma SH-SY5Y cells. The addition of gnetin C (10 μM) to the media moderately reduced the CCL2 production and markedly suppressed CCL5 production in both cells. In the TLR3-interferon (IFN)-β-phosphorylated-STAT1 (signal transducer and activator of transcription protein 1)-RIG-I (retinoic acid-inducible gene-I) pathway that mediates CCL2 and CCL5 production, gnetin C first inhibits IFN-β expression in SH-SY5Y cells and primarily inhibits STAT1 phosphorylation in U373MG cells. In any case, gnetin C attenuated the dsRNA-activated TLR3 signaling resulting in CCL2 and CCL5 production, thus, may be useful for controlling TLR3-mediated inflammation in the brain.

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Section: Time-and Concentration-dependent Poly Ic-induced Mrna Expressupporting

confidence: 75%

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confidence: 99%

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confidence: 99%

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confidence: 99%

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Gnetin C suppresses double-stranded RNA-induced C-C motif chemokine ligand 2 (CCL2) and CCL5 production by inhibiting Toll-like receptor 3 signaling pathway

et al. 2018

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“…MDA5 was identified as a gene associated with the differentiation of melanoma cells . RIG‐I and MDA5 function as cytoplasmic receptors for dsRNA, and also as signaling molecules that regulate C‐X‐C motif chemokine ligand 10 (CXCL10) expression in U373MG cells, a cell line derived from astrocytoma . We have previously shown that poly IC induces RIG‐I in human umbilical vein endothelial cells, and experimental inoculation of the hantavirus into rats enhances RIG‐I expression in thalamus endothelial cells .…”

Section: Introductionmentioning

confidence: 99%

Retinoic acid‐inducible gene‐I, melanoma differentiation‐associated gene 5 and C‐X‐C motif chemokine ligand 10 are induced by a Toll‐like receptor 3 agonist in human brain microvascular endothelial cells

Imaizumi¹,

Arai²,

Kawaguchi

et al. 2018

Clinical & Exp Neuroim

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Objective Brain microvascular endothelial cells (BMEC) are the major component of the blood-brain barrier, and play a critical role in protecting the brain from pathogens. Although Toll-like receptor 3 (TLR3) is known as an important pattern-recognition receptor against viral double-stranded RNA, the downstream reactions of TLR3 in human BMEC are not fully characterized. The purpose of the present study was to investigate the role of TLR3 signaling in the expression of retinoic acid-inducible gene-I (RIG-I), melanoma differentiation-associated gene 5 (MDA5) and C-X-C motif chemokine ligand 10 (CXCL10) in human BMEC. Methods The hCMEC/D3 cells, a human BMEC cell line, were cultured and stimulated with polyinosinic-polycytidylic acid, a synthetic TLR3 agonist. Quantitative real-time reverse transcription polymerase chain reaction, western blotting and enzyme-linked immunosorbent assay were used to examine the expression of interferon-b, RIG-I and CXCL10. RNA interference against TLR3, interferon-b, RIG-I or MDA5 was also carried out. Results Expression of RIG-I, MDA5 and CXCL10 were induced by polyinosinic-polycytidylic acid, and this was inhibited by knockdown of either TLR3 or interferon-b. Knockdown of RIG-I or MDA5 did not affect the CXCL10 expression in the early phase (4 h), but decreased the CXCL10 induction in the late phase (8 or 24 h). Conclusions RIG-I, MDA5 and CXCL10 are induced through TLR3 activation in hCMEC/D3 cells, and RIG-I and MDA5 might function to enhance and/or prolong the reactions mediated by CXCL10. These molecules might play a distinct role in innate immune reactions against double-stranded RNA viruses in human BMEC.

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Targeting SOX2 Protein with Peptide Aptamers for Therapeutic Gains against Esophageal Squamous Cell Carcinoma

et al. 2020

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Interferon (IFN)-induced protein 35 (IFI35) negatively regulates IFN-β-phosphorylated STAT1-RIG-I-CXCL10/CCL5 axis in U373MG astrocytoma cells treated with polyinosinic-polycytidylic acid

Cited by 21 publications

References 29 publications

<b>Gnetin C suppresses double-stranded RNA-induced C-C motif chemokine ligand 2 (CCL2) and CCL5 production by inhibiting Toll-like receptor 3 signaling </b><b>pathway </b>

<b>Gnetin C suppresses double-stranded RNA-induced C-C motif chemokine ligand 2 (CCL2) and CCL5 production by inhibiting Toll-like receptor 3 signaling </b><b>pathway </b>

Retinoic acid‐inducible gene‐I, melanoma differentiation‐associated gene 5 and C‐X‐C motif chemokine ligand 10 are induced by a Toll‐like receptor 3 agonist in human brain microvascular endothelial cells

Targeting SOX2 Protein with Peptide Aptamers for Therapeutic Gains against Esophageal Squamous Cell Carcinoma

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