CoChat
Sign Up
Cited by 220

The DOI matches its Crossref record; 2 of the 2 references it cites were found in a registry or an index.

Inhibition of TLR4 Induces M2 Microglial Polarization and Provides Neuroprotection via the NLRP3 Inflammasome in Alzheimer’s Disease

Cui, Weigang, Sun, Chunli, Ma, Yuqi, Wang, Songtao, Wang, Xianwei, Zhang, Yinghua·2020·Frontiers in Neuroscience
DOI 10.3389/fnins.2020.00444PMC PMC7251077
Open this paper in CoChat — free account

Overview

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.3389/fnins.2020.00444

Cites

2 of 2 references verified0 citation errors · 0 not checkable

Statistics

Figures

FIGURE 1 TLR4 expressions were increased in the APP/PS1 Transgenic Mice. TLR4 levels in 6-month-old APP/PS1 transgenic and WT mice were shown by Western blot (A). Confocal analysis for Aβ (red) and TLR4 (green) revealed that Aβ deposition was surrounded by TLR4-positive cells in APP/PS1 transgenic AD mice (B). TLR4 (green) colocalized with CD11b (red) (C), which is indicated by an arrow. Scale bar: 20 μm. GAPDH was used as a loading control, and the densitometry was quantified. Data were analyzed with Student’s t-test. Data are expressed as mean ± SD, n = 5 for each group (∗∗P < 0.01 compared with the WT mice).
FIGURE 1 TLR4 expressions were increased in the APP/PS1 Transgenic Mice. TLR4 levels in 6-month-old APP/PS1 transgenic and WT mice were shown by Western blot (A). Confocal analysis for Aβ (red) and TLR4 (green) revealed that Aβ deposition was surrounded by TLR4-positive cells in APP/PS1 transgenic AD mice (B). TLR4 (green) colocalized with CD11b (red) (C), which is indicated by an arrow. Scale bar: 20 μm. GAPDH was used as a loading control, and the densitometry was quantified. Data were analyzed with Student’s t-test. Data are expressed as mean ± SD, n = 5 for each group (∗∗P < 0.01 compared with the WT mice).CC BY · PubMed Central
FIGURE 2 Microglial morphological changes in the PFC in APP/PS1 AD mice and its regulation by TAK-242 treatment. Representative immunofluorescence staining images show CD11b-positive microglia in the PFC of WT mice (A) and APP/PS1 transgenic mice (B). Morphological changes were suppressed by treatment with TAK-242, as shown in the immunofluorescence staining of vehicle (C) and TAK-242 (D) treatments. Hypertrophic morphology with thick microglial processes is indicated by an arrow. Panels (E) and (F) are magnifications of the rectangular region indicated in parts A and B, Scale bar: 5 μm. The area of CD11b positive reactivity is presented (G). The percentage of amoeboid microglial cells over the total microglial cells for each experimental group is presented (H). Data were analyzed with one-way ANOVA followed by post hoc Bonferroni test analysis. Data are expressed as mean ± SD, n = 5 for each group (∗∗P < 0.01, ∗∗∗P < 0.001 compared with the WT mice group. ##P < 0.01 compared with the Vehicle-treated control group).
FIGURE 2 Microglial morphological changes in the PFC in APP/PS1 AD mice and its regulation by TAK-242 treatment. Representative immunofluorescence staining images show CD11b-positive microglia in the PFC of WT mice (A) and APP/PS1 transgenic mice (B). Morphological changes were suppressed by treatment with TAK-242, as shown in the immunofluorescence staining of vehicle (C) and TAK-242 (D) treatments. Hypertrophic morphology with thick microglial processes is indicated by an arrow. Panels (E) and (F) are magnifications of the rectangular region indicated in parts A and B, Scale bar: 5 μm. The area of CD11b positive reactivity is presented (G). The percentage of amoeboid microglial cells over the total microglial cells for each experimental group is presented (H). Data were analyzed with one-way ANOVA followed by post hoc Bonferroni test analysis. Data are expressed as mean ± SD, n = 5 for each group (∗∗P < 0.01, ∗∗∗P < 0.001 compared with the WT mice group. ##P < 0.01 compared with the Vehicle-treated control group).CC BY · PubMed Central
FIGURE 3 M1- and M2-microglia associated markers and MyD88, NF-κB p65, and NLRP3 signaling were altered after TAK-242 treatment in APP/PS1 transgenic mice. ELISA analysis for the M1-microglia-associated markers iNOS and TNFα (A,B) and the M2-microglia-associated markers TREM-2 and Arg-1 (C,D). TAK-242 decreased the expression of MyD88, NF-κB p65, and NLRP3 (E–H). GAPDH was used as a loading control. Data were analyzed with Student’s t-test. Data are expressed as mean ± SD, n = 5 for each group (∗significant as compared with vehicle-treated control group, ∗∗P < 0.01, ∗∗∗P < 0.001).
FIGURE 3 M1- and M2-microglia associated markers and MyD88, NF-κB p65, and NLRP3 signaling were altered after TAK-242 treatment in APP/PS1 transgenic mice. ELISA analysis for the M1-microglia-associated markers iNOS and TNFα (A,B) and the M2-microglia-associated markers TREM-2 and Arg-1 (C,D). TAK-242 decreased the expression of MyD88, NF-κB p65, and NLRP3 (E–H). GAPDH was used as a loading control. Data were analyzed with Student’s t-test. Data are expressed as mean ± SD, n = 5 for each group (∗significant as compared with vehicle-treated control group, ∗∗P < 0.01, ∗∗∗P < 0.001).CC BY · PubMed Central
FIGURE 4 TLR4 inhibition treatment ameliorated impaired performance, decreased Aβ deposition, and exerted an anti-apoptosis effect in AD mice. The vehicle-treated group exhibited longer escape latencies to reach the hidden platform compared with TAK-242-treated mice (A), P < 0.05 by repeated-measure two-way ANOVA (Veh, n = 13; TAK-242, n = 13). The number of times of crossing the platform are shown (B), ∗∗P < 0.01 compared with the vehicle-treated group (Student’s t-test). No differences in the swim speeds or total distance (C,D) were found in TLR4 inhibition group compared with vehicle-treatment group. TAK-242 reduced the amyloid load in PFC and HC as the percentage of surface coverage (E,F), Scale bar 60 μm. TLR4 inhibition decreased the expression of Bax and the extent of DNA fragmentation (G–I), Data were analyzed with Student’s t-test. Data are expressed as mean ± SD. ∗∗P < 0.01, compared with vehicle-treated control.
FIGURE 4 TLR4 inhibition treatment ameliorated impaired performance, decreased Aβ deposition, and exerted an anti-apoptosis effect in AD mice. The vehicle-treated group exhibited longer escape latencies to reach the hidden platform compared with TAK-242-treated mice (A), P < 0.05 by repeated-measure two-way ANOVA (Veh, n = 13; TAK-242, n = 13). The number of times of crossing the platform are shown (B), ∗∗P < 0.01 compared with the vehicle-treated group (Student’s t-test). No differences in the swim speeds or total distance (C,D) were found in TLR4 inhibition group compared with vehicle-treatment group. TAK-242 reduced the amyloid load in PFC and HC as the percentage of surface coverage (E,F), Scale bar 60 μm. TLR4 inhibition decreased the expression of Bax and the extent of DNA fragmentation (G–I), Data were analyzed with Student’s t-test. Data are expressed as mean ± SD. ∗∗P < 0.01, compared with vehicle-treated control.CC BY · PubMed Central
FIGURE 5 TAK-242 regulated Aβ-induced M1 and M2 inflammatory microglia polarization. BV2 microglia were treated with various concentrations of TAK-242 for 24 h, and the cell viability was then measured by MTT assays (A). The optimal dose of TAK-242 in inhibiting Aβ-induced inflammation response was analyzed by ELISA assay (B). The expressions of iNOS, TNFα, TREM-2, and Arg-1 (C–F) were measured by ELISA kit. Data were analyzed with Student’s t-test or one-way ANOVA followed by post hoc Bonferroni test analysis. All the experiments were repeated three times (n = 5). Data are expressed as mean ± SD (∗P < 0.05, ∗∗P < 0.01, ∗∗∗P < 0.001 compared with the Vehicle-treated control group. ##P < 0.01 compared with the Aβ25–35 (25 μM)-treated group).
FIGURE 5 TAK-242 regulated Aβ-induced M1 and M2 inflammatory microglia polarization. BV2 microglia were treated with various concentrations of TAK-242 for 24 h, and the cell viability was then measured by MTT assays (A). The optimal dose of TAK-242 in inhibiting Aβ-induced inflammation response was analyzed by ELISA assay (B). The expressions of iNOS, TNFα, TREM-2, and Arg-1 (C–F) were measured by ELISA kit. Data were analyzed with Student’s t-test or one-way ANOVA followed by post hoc Bonferroni test analysis. All the experiments were repeated three times (n = 5). Data are expressed as mean ± SD (∗P < 0.05, ∗∗P < 0.01, ∗∗∗P < 0.001 compared with the Vehicle-treated control group. ##P < 0.01 compared with the Aβ25–35 (25 μM)-treated group).CC BY · PubMed Central
FIGURE 6 TAK-242 promoted microglial phagocytosis. The purity of the BV2 cell line was identified by immunostaining with an CD11b antibody specific to microglia (A–C). Scale bar: 20 μm. Compared with Aβ-treated control cells, the effect of TAK-242 on microglial phagocytosis was assessed by the number of fluorescent microbeads (yellow) in cells. CD11b-labeled microglia are shown in red, and DAPI-labeled cell nuclei are shown in blue. Fluorescent microbeads in yellow are indicated by an arrow (D,E). Scale bar: 20 μm. Data were analyzed with one-way ANOVA followed by post hoc Bonferroni test analysis. All the experiments were repeated three times (n = 5). Data are expressed as mean ± SD (∗∗∗P < 0.001 compared with the Vehicle treated group. ###P < 0.001 compared with the Aβ25–35 (25 μM)-treated group).
FIGURE 6 TAK-242 promoted microglial phagocytosis. The purity of the BV2 cell line was identified by immunostaining with an CD11b antibody specific to microglia (A–C). Scale bar: 20 μm. Compared with Aβ-treated control cells, the effect of TAK-242 on microglial phagocytosis was assessed by the number of fluorescent microbeads (yellow) in cells. CD11b-labeled microglia are shown in red, and DAPI-labeled cell nuclei are shown in blue. Fluorescent microbeads in yellow are indicated by an arrow (D,E). Scale bar: 20 μm. Data were analyzed with one-way ANOVA followed by post hoc Bonferroni test analysis. All the experiments were repeated three times (n = 5). Data are expressed as mean ± SD (∗∗∗P < 0.001 compared with the Vehicle treated group. ###P < 0.001 compared with the Aβ25–35 (25 μM)-treated group).CC BY · PubMed Central
FIGURE 7 TAK-242 suppressed Aβ-induced MyD88/NF-κB p65 and NLRP3 inflammasome activation and Aβ-induced apoptosis in BV2 microglial cells. TAK-242 suppressed the expression of MyD88 NF-κB p65 and NLRP3 by Western blot (A,B). TAK-242 treatment decreased the level of Bax and DNA fragmentation in SH-SY5Y cells (C,D) and in primary neuronal cells (E,F). GAPDH was used as a loading control. Data were analyzed with one-way ANOVA followed by post hoc Bonferroni test analysis. All the experiments were repeated three times (n = 5). Data are expressed as mean ± SD (∗∗P < 0.01, ∗∗∗P < 0.001 compared with the Vehicle treated group. ##P < 0.01, ###P < 0.001 compared with the Aβ25–35 (25 μM)-treated group).
FIGURE 7 TAK-242 suppressed Aβ-induced MyD88/NF-κB p65 and NLRP3 inflammasome activation and Aβ-induced apoptosis in BV2 microglial cells. TAK-242 suppressed the expression of MyD88 NF-κB p65 and NLRP3 by Western blot (A,B). TAK-242 treatment decreased the level of Bax and DNA fragmentation in SH-SY5Y cells (C,D) and in primary neuronal cells (E,F). GAPDH was used as a loading control. Data were analyzed with one-way ANOVA followed by post hoc Bonferroni test analysis. All the experiments were repeated three times (n = 5). Data are expressed as mean ± SD (∗∗P < 0.01, ∗∗∗P < 0.001 compared with the Vehicle treated group. ##P < 0.01, ###P < 0.001 compared with the Aβ25–35 (25 μM)-treated group).CC BY · PubMed Central
FIGURE 8 Effects of NLRP3 Gene Silencing on Aβ-Induced M1 and M2 inflammatory microglial polarization. (A,B) BV2 cells transfected with control or NLRP3-specific siRNA for 48 h. The relative levels of NLRP3 to GADPH protein expression were determined by Western blot. Knockdown of NLRP3 mRNA by NLRP3 siRNA in BV2 microglia significantly mitigated Aβ-induced levels on M1 markers (iNOS and TNFα) (C,D), and the Aβ-induced levels of iNOS and TNFα were also mitigated by TAK-242 treatment. Consistent with these findings, increases in TREM-2 and Arg-1 expressions were facilitated by treating siRNA-NLRP3 (E,F) in cultured supernatant, as measured by ELISA. Data were analyzed with one-way ANOVA followed by post hoc Bonferroni test analysis. All the experiments were repeated three times (n = 5). Data are expressed as mean ± SD (∗significant as compared with the vehicle-treated group, ∗∗∗P < 0.001. #significant as compared with the Aβ25-35 (25 μM)-treated group, #P < 0.05. $Significant as compared with the Aβ + siRNA NLRP3-treated group, $P < 0.05).
FIGURE 8 Effects of NLRP3 Gene Silencing on Aβ-Induced M1 and M2 inflammatory microglial polarization. (A,B) BV2 cells transfected with control or NLRP3-specific siRNA for 48 h. The relative levels of NLRP3 to GADPH protein expression were determined by Western blot. Knockdown of NLRP3 mRNA by NLRP3 siRNA in BV2 microglia significantly mitigated Aβ-induced levels on M1 markers (iNOS and TNFα) (C,D), and the Aβ-induced levels of iNOS and TNFα were also mitigated by TAK-242 treatment. Consistent with these findings, increases in TREM-2 and Arg-1 expressions were facilitated by treating siRNA-NLRP3 (E,F) in cultured supernatant, as measured by ELISA. Data were analyzed with one-way ANOVA followed by post hoc Bonferroni test analysis. All the experiments were repeated three times (n = 5). Data are expressed as mean ± SD (∗significant as compared with the vehicle-treated group, ∗∗∗P < 0.001. #significant as compared with the Aβ25-35 (25 μM)-treated group, #P < 0.05. $Significant as compared with the Aβ + siRNA NLRP3-treated group, $P < 0.05).CC BY · PubMed Central

Verification

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Citations

Cites

Show all 2 references

Research works printed but not linked: 45

  1. Al, 2018, Interferon regulatory factor 4/5 signaling impacts on microglial activation after ischemic stroke in mice., Eur. J. Neurosci., 47, 140, 10.1111/ejn.13778 · DOI
  2. Aryanpour, 2017, Progesterone therapy induces an M1 to M2 switch in microglia phenotype and suppresses NLRP3 inflammasome in a cuprizone-induced demyelination mouse model., Int. Immunopharmacol., 51, 131, 10.1016/j.intimp.2017.08.007 · DOI
  3. Oliveira, 2018, Inflammation as a possible link between dyslipidemia and Alzheimer’s disease., Neuroscience, 376, 127, 10.1016/j.neuroscience.2018.02.012 · DOI
  4. Businaro, 2018, Modulation of inflammation as a way of delaying Alzheimer’s disease progression: the Diet’s role., Curr Alzheimer Res, 15, 363, 10.2174/1567205014666170829100100 · DOI
  5. Cui, 2012, Liver X receptor activation attenuates inflammatory response and protects cholinergic neurons in APP/PS1 transgenic mice., Neuroscience, 210, 200, 10.1016/j.neuroscience.2012.02.047 · DOI
  6. Cui, 2013, Neuregulin1beta1 antagonizes apoptosis via ErbB4-dependent activation of PI3-kinase/Akt in APP/PS1 transgenic mice., Neurochem. Res., 38, 2237, 10.1007/s11064-013-1131-z · DOI
  7. Cui, 2017, Inhibition of PTEN attenuates endoplasmic reticulum stress and apoptosis via activation of PI3K/AKT pathway in Alzheimer’s disease., Neurochem. Res., 42, 3052, 10.1007/s11064-017-2338-1 · DOI
  8. Fahnestock, 2019, ProNGF and neurodegeneration in Alzheimer’s disease., Front. Neurosci., 13, 10.3389/fnins.2019.00129 · DOI
  9. Fiala, 2018, Immunotherapy of mild cognitive impairment by omega-3 supplementation: why are Amyloid-beta Antibodies and omega-3 not working in clinical trials., J. Alzheimers Dis., 62, 1013, 10.3233/JAD-170579 · DOI · Paper page
  10. Henn, 2009, The suitability of BV2 cells as alternative model system for primary microglia cultures or for animal experiments examining brain inflammation., ALTEX, 26, 83, 10.1016/j.jmpt.2008.11.018 · DOI
  11. Hu, 2017, Inhibition of TLR4 alleviates the inflammation and apoptosis of retinal ganglion cells in high glucose., Graefes Arch. Clin. Exp. Ophthalmol., 255, 2199, 10.1007/s00417-017-3772-0 · DOI
  12. Hu, 2012, Microglia/macrophage polarization dynamics reveal novel mechanism of injury expansion after focal cerebral ischemia., Stroke, 43, 3063, 10.1161/STROKEAHA.112.659656 · DOI
  13. Hua, 2015, TAK-242, an antagonist for Toll-like receptor 4, protects against acute cerebral ischemia/reperfusion injury in mice., J. Cereb. Blood Flow Metab., 35, 536, 10.1038/jcbfm.2014.240 · DOI
  14. Huang, 2017, TLR4 is a link between diabetes and Alzheimer’s disease., Behav. Brain Res., 316, 234, 10.1016/j.bbr.2016.08.047 · DOI
  15. Jankowsky, 2004, Mutant presenilins specifically elevate the levels of the 42 residue beta-amyloid peptide in vivo: evidence for augmentation of a 42-specific gamma secretase., Hum. Mol. Genet., 13, 159, 10.1093/hmg/ddh019 · DOI · Paper page
  16. Latta-Mahieu, 2018, Systemic immune-checkpoint blockade with anti-PD1 antibodies does not alter cerebral amyloid-beta burden in several amyloid transgenic mouse models., Glia, 66, 492, 10.1002/glia.23260 · DOI
  17. Li, 2014, Role of the TLR4 pathway in blood-spinal cord barrier dysfunction during the bimodal stage after ischemia/reperfusion injury in rats., J. Neuroinflam., 11, 10.1186/1742-2094-11-62 · DOI
  18. Lu, 2018, Quercetin ameliorates kidney injury and fibrosis by modulating M1/M2 macrophage polarization., Biochem. Pharmacol., 154, 203, 10.1016/j.bcp.2018.05.007 · DOI
  19. Ma, 2018, LncRNA XIST mediates bovine mammary epithelial cell inflammatory response via NF-kappaB/NLRP3 inflammasome pathway., Cell Prolif., 52, 10.1111/cpr.12525 · DOI
  20. Maezawa, 2018, Kv1.3 inhibition as a potential microglia-targeted therapy for Alzheimer’s disease: preclinical proof of concept., Brain, 141, 596, 10.1093/brain/awx346 · DOI · Paper page
  21. Matsunaga, 2011, TAK-242 (resatorvid), a small-molecule inhibitor of Toll-like receptor (TLR) 4 signaling, binds selectively to TLR4 and interferes with interactions between TLR4 and its adaptor molecules., Mol. Pharmacol., 79, 34, 10.1124/mol.110.068064 · DOI · Paper page
  22. McCarthy, 2016, Characterization of a novel adult murine immortalized microglial cell line and its activation by amyloid-beta., J. Neuroinflam., 13, 10.1186/s12974-016-0484-z · DOI
  23. McClain, 2011, Adolescent binge alcohol exposure induces long-lasting partial activation of microglia., Brain Behav. Immun., S120, 10.1016/j.bbi.2011.01.006 · DOI
  24. Miron, 2018, TLR4 gene expression and pro-inflammatory cytokines in Alzheimer’s disease and in response to hippocampal deafferentation in rodents., J. Alzheimers Dis., 63, 1547, 10.3233/JAD-171160 · DOI · Paper page
  25. Mohammad, 2018, Reno-protective effects of TAK-242 on acute kidney injury in a rat model., Biochem. Biophys. Res. Commun., 503, 304, 10.1016/j.bbrc.2018.06.020 · DOI
  26. Moser, 2018, TLR4 inhibitor TAK-242 attenuates the adverse neural effects of diet-induced obesity., J. Neuroinflam., 15, 10.1186/s12974-018-1340-0 · DOI
  27. O’Halloran, 2014, MyD88 acts as an adaptor protein for inflammatory signalling induced by amyloid-beta in macrophages., Immunol. Lett., 162, 109, 10.1016/j.imlet.2014.08.001 · DOI
  28. Rosciszewski, 2018, Toll-Like Receptor 4 (TLR4) AND TRIGGERING RECEPTOR EXPRESSED ON Myeloid Cells-2 (TREM-2) activation balance astrocyte polarization into a proinflammatory phenotype., Mol. Neurobiol., 55, 3875
  29. Saresella, 2014, A complex proinflammatory role for peripheral monocytes in Alzheimer’s disease., J. Alzheimers Dis., 38, 403, 10.3233/JAD-131160 · DOI
  30. Shi, 2013, Prion protein participates in the regulation of classical and alternative activation of BV2 microglia., J. Neurochem., 124, 168, 10.1111/jnc.12053 · DOI
  31. Shibata, 2017, Toll-like receptor 4 antagonist TAK-242 inhibits autoinflammatory symptoms in DITRA., J. Autoimmun., 80, 28, 10.1016/j.jaut.2017.01.007 · DOI
  32. Song, 2018, Knockdown of NLRP3 alleviates high glucose or TGFB1-induced EMT in human renal tubular cells., J. Mol. Endocrinol., 61, 101, 10.1530/JME-18-0069 · DOI
  33. Su, 2018, Inhibition of toll-like receptor 4 alleviates hyperalgesia induced by acute dural inflammation in experimental migraine., Mol. Pain, 14, 1, 10.1177/1744806918754612 · DOI
  34. Su, 2018, Effects of the TLR4/Myd88/NF-kappaB Signaling Pathway on NLRP3 inflammasome in coronary microembolization-induced myocardial injury., Cell. Physiol. Biochem., 47, 1497, 10.1159/000490866 · DOI
  35. Tai, 2018, Magnesium Lithospermate B suppresses lipopolysaccharide-induced neuroinflammation in BV2 Microglial cells and attenuates neurodegeneration in Lipopolysaccharide-injected mice., J. Mol. Neurosci., 64, 80, 10.1007/s12031-017-1007-9 · DOI
  36. Tan, 2013, The NLRP3 inflammasome in Alzheimer’s disease., Mol. Neurobiol., 48, 875, 10.1007/s12035-013-8475-x · DOI
  37. Tao, 2018, Andrographolide alleviates acute brain injury in a rat model of traumatic brain injury: possible involvement of inflammatory signaling., Front. Neurosci., 12, 10.3389/fnins.2018.00657 · DOI
  38. Tramullas, 2016, Obesity takes its toll on Visceral pain: high-Fat diet induces toll-like receptor 4-Dependent Visceral hypersensitivity., PLoS One, 11, 10.1371/journal.pone.0155367 · DOI
  39. Wang, 2017, TAK-242 protects against apoptosis in Coronary Microembolization-INDUCED MYOCARDIAL INJURY IN RATS BY SUPPRESSING TLR4/NF-kappaB signaling pathway., Cell. Physiol. Biochem., 41, 1675, 10.1159/000471248 · DOI
  40. Xie, 2016, Protective Effect of 2-Dodecyl-6-Methoxycyclohexa-2, 5-Diene-1, 4-Dione, isolated from Averrhoa Carambola L., Against Palmitic Acid-Induced Inflammation and Apoptosis in Min6 Cells by Inhibiting the TLR4-MyD88-NF-kappaB Signaling Pathway., Cell Physiol. Biochem., 39, 1705, 10.1159/000447871 · DOI
  41. Yang, 2018, Toll-like receptor 4-induced ryanodine receptor 2 oxidation and sarcoplasmic reticulum Ca(2+) leakage promote cardiac contractile dysfunction in sepsis., J. Biol. Chem., 293, 794, 10.1074/jbc.M117.812289 · DOI
  42. Zhang, 2017, Acute Hypoxia Induced an Imbalanced M1/M2 Activation of Microglia through NF-kappaB Signaling in Alzheimer’s Disease Mice and Wild-Type Littermates., Front. Aging Neurosci, 9, 10.3389/fnagi.2017.00282 · DOI
  43. Zhang, 2015, TAK-242, a Toll-Like receptor 4 antagonist, protects against Aldosterone-Induced cardiac and renal injury., PLoS One, 10, 10.1371/journal.pone.0142456 · DOI
  44. Zhao, 2016, Inhibition of TLR4 signalling-induced inflammation attenuates secondary injury after diffuse axonal injury in rats., Mediators Inflamm., 2016, 10.1155/2016/4706915 · DOI
  45. Zhou, 2017, Astragalus polysaccharides exerts immunomodulatory effects via TLR4-mediated MyD88-dependent signaling pathway in vitro and in vivo., Sci. Rep., 7, 10.1038/srep44822 · DOI

Cited by

Sorted by citations

Metadata

Authors
Cui, W., Sun, C., Ma, Y., Wang, S., Wang, X., & Zhang, Y.
Venue
Frontiers in Neuroscience
Publisher
Frontiers Media SA
Published
2020-05-20
Volume
14
ISSN
1662-453X
DOI
10.3389/fnins.2020.00444
PMC
PMC7251077
Cited by
220
References
2
Licence
creativecommons.org/licenses/by/4.0/ (vor)
Funders
  • National Natural Science Foundation of China (U1804185, 81873459, U1804166)
  • Science and Technology Department of Henan Province (192102310346)

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review