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Table 1 The direct link between TLR4 and miR-155 in the context of different disorders or cell lines

From: TLR4 signaling in the development of colitis-associated cancer and its possible interplay with microRNA-155

  Cells/tissues types used in in vivo/in vitro studies Intervention Dose and time course of intervention Main related outcomes Measurement methods used to determine the main related outcomes The studied disease conditions References
Regulatory activity of miR-155 on TLR4 signaling Human HaCaT keratinocytes miR-155 mimic transfection 100 ng for 6 h TLR4 expression was significantly increased by miR-155 overexpression Western blot Psoriasis [90]
  Mouse microglia BV2 cells miR-155 mimic transfection 1 μmol/L for 24 h Oxygen–glucose deprivation-induced TLR4 upregulation was promoted and inhibited, respectively, by miR-155 overexpression and knockdown Western blot Ischemic brain injury [92]
   miR-155 inhibitor transfection 2 μmol/L for 24 h    
  Human acute mono-cytic leukemia THP-1 cells and THP-1-derived macrophages miR-155-3p mimic transfection 15 nM for 12 h TLR4 was downregulated by miR-155-3p in monocytes and macrophages qPCR – [89]
  Mouse brain tissues miR-155−/− mice Model animal Marked expression of TLR4 was observed in ischemic cerebral tissue of WT mice at 24 h after middle cerebral artery occlusion, and this expression was obviously reduced in miR-155−/− mice Western blot /qPCR Ischemic brain injury [92]
   Injection of pAdmiR-155 into lateral cerebral ventricle of mice Single stereotactic injection TLR4 expression was significantly increased in ischemic cerebral tissue of miR-155-overexpressing mice compared with pAd-infected mice Western blot /qPCR   
  Mouse prostate tissues miR-155−/− mice Model animal miR-155−/− mice with prostatitis exhibited the suppressed TLR4/NF-κB pathway as compared with the WT mice with prostatitis Western blot Experimental autoimmune prostatitis [91]
Inductive effect of TLR4 activation on miR-155 Mouse RAW264.7 cells LPS treatment 100 ng/mL for 0–24 h Among the miRNAs that were induced the most by LPS, miR-155 was on the top of the list MicroRNA arrays – [93, 105, 106, 110, 123, 135, 136]
     It was validated that miR-155 and BIC/primiR-155 expression was increased in a time-dependent manner Northern blot/qPCR   
    0–1 μg/mL for 24 h miR-155 and BIC expression was increased in a dose-dependent manner qPCR   
    100 ng/mL for 24 h In cells transfected with pri-155 promoter, pri-155 promoter was drove fivefold by LPS Luciferase assay   
    10 ng/mL for 6 h Among the LPS-induced miRNAs, miR-155 showed the highest fold change (40-fold) MicroRNA deep-sequencing   
  Mouse BMDMs LPS treatment 100 ng/mL for 0–24 h The time-dependent induction of BIC transcript and miR-155 by LPS was observed in BMDMs from WT mice Northern blot/qPCR – [93, 105, 110, 123, 129, 135, 136]
    0–0.1 μg/mL for 8 h miR-155 expression was increased in a dose-dependent manner qPCR   
    100 ng/mL for 8 h A strong and prolonged increase of miR-155 expression was induced by LPS in BMDMs without a concomitant increase of pri-miR155 Northern blot/Semi-quantitative RT-PCR   
   TLR4−/− BMDM Model cell LPS-induced miR-155 expression was decreased from approximately 40-fold activation in WT-BMDM to less than twofold in TLR4−/− BMDM qPCR   
  Human PBMCs LPS treatment 100 ng/mL for 0–24 h miR-155 expression was increased eightfold by LPS in PBMC after 24 h stimulation qPCR – [93, 135]
  Human monocytes LPS treatment 100 ng/mL for 6 and 24 h miR-155 expression was upregulated by LPS at both timepoints MicroRNAdeep-sequencing/qPCR – [109]
  Mouse bone marrow-derived DCs LPS treatment 1 ug/mL for 24 h In response to stimulation with LPS, miR-155 expression was upregulated in mature DCs as compared with immature DCs MicroRNA arrays/qPCR – [108]
  Human monocyte-derived DCs LPS treatment 1 ug/mL for 24 h At 24 h after stimulation, miR-155 expression was upregulated by LPS when compared to cells receiving medium alone qPCR – [107]
  Human monocyte-derived Macrophage LPS treatment 100 ng/mL for 24 h An increase of miR-155-5p levels induced by LPS was found in monocyte- derived macrophage (fold change ~ 60) qPCR – [132]
  Mouse primary microglia LPS treatment 0.1 or 1 μg/mL for 18 h LPS treatment at the level of 0.1 or 1 μg/mL lead to a 12-fold or 21-fold increase in the expression of miR-155, respectively qPCR Ischemic brain injury [111, 113]
     The miR-155 labelling was significantly more intense in the cytoplasm of microglia cells incubated with LPS than in control cells In situ hybridization   
  Mouse microglia N9 cells LPS treatment 0.1, 0.5 and 1 μg/mL for 18 h and 0.1 μg/mL for different time periods (0.5, 1, 2, 4, 18 and 24 h) miR-155 expression was induced in a dose-dependent manner, which reached a 25-fold increase in miR-155 levels for the highest LPS concentration tested qPCR Ischemic brain injury [111]
     miR-155 levels continued to increase, reaching a maximum at 18 h, but showed a tendency to decrease after an incubation period of 24 h    
  Mouse microglia BV2 cells LPS treatment 100 ng/mLfor 4 h miR-155-3p was the most significantly upregulated miRNA (by 29-fold versus control), followed by miR-155-5p (by 9.7-fold) MicroRNA sequencing Brain injury [112, 113]
    20 ng/mL for 24 h miR-155 expression was significantly increased qPCR   
  Mouse kupffer cells (KCs) LPS treatment 100 ng/mL for 6 and 18 h Alcohol-induced miR-155 expression was further augmented by in vitro LPS challenge in KCs isolated from alcohol-fed mice compared with pair-fed mice qPCR Alcoholic steatohepatitis [100, 133]
  Mouse alveolar macrophages (AMs) LPS treatment 100 ng/mL for indicated time periods (0–6 h) miR-155 expression level was dramatically increased in response to LPS stimulation in control AMs qPCR Acute lung injury [128]
  Human proximal tubule epithelial HK-2 cells LPS treatment 5 μg/mL for 24 h miR-155 expression was significantly elevated qPCR Acute kidney injury [114, 115]
  Rat synovial fibroblast LPS treatment 1 mg/L for 24 h miR-155 expression was significantly higher in the LPS-treated group than in control group qPCR Rheumatoid arthritis [116]
  Human umbilical vein endothelial cells LPS treatment 0.05, 0.1 and 1 μg/L for 24 h The expression of miR-155 was enhanced by LPS in a dose dependent manner qPCR – [117]
  Mouse osteoblasts LPS treatment 50 ng/mL for 0–48 h miR-155 expression was upregulated in a time-dependent manner, reached a peak at 24 h qPCR Osteomyelitis [118]
  Mouse pre-osteoblast MC3T3-E1 cells LPS treatment 100 and 200 ng/mL for 0–48 h The level of miR-155 was significantly upregulated in a time-dependent manner upon LPS stimulation compared to the control qPCR Osteomyelitis [119]
  Mouse osteoclasts LPS treatment 50 ng/mL for 24 and 48 h The expression level of miR-155 was low in pre-OCs, whereas it was up-regulated upon LPS stimulation > 140-fold at 24 h and maintained it up to 48 h qPCR Inflammatory bone loss [118]
  Human breast cancer MCF-7 cells LPS treatment 5 ng/mL for 6 and 12 h The level of miR-155 expression was about threefold higher at 6 h after LPS stimulation qPCR Breast cancer [120]
  Human B-lymphoma BJAB cells LPS treatment 5 μg/mL for 6 and 24 h miR-155 levels were increased by ∼twofold after 6 h of LPS treatment and by ~ threefold at 24 h qPCR B-cell lymphoma [121]
     Treatment of BJAB cells with LPS for 6 h caused a significant increase in BIC mRNA levels and BIC mRNA remained elevated after 24 h treatment Semi-quantitative RT-PCR   
  Mouse Insulinoma MIN6 Cells LPS treatment 5, 20, or 50 ng/mL for 6 h miR-155-5p expression was increased qPCR – [122]
  Human islet cells LPS treatment 5 or 50 ng/mL for 6 h miR-155-5p expression was increased qPCR – [122]
  Human bronchial epithelial 16HBE cells LPS treatment 1 μg/mL for 6 h miR-155 expression was induced by activation of TLR4 by LPS qPCR Chronic airway inflammatory diseases [124]
  Human intestinal myofibroblasts (IMF) LPS treatment 1 μg/mL for 72 h LPS increased miR-155 level following 72 h exposure in control-derived IMF and further upregulated miR-155 level in UC-derived IMF qPCR Ulcerative colitis [131]
  Human trophoblast HTR-8/SVneo cells LPS treatment 0–800 ng/mL for 0.5–48 h miR-155 was increased in a time- and dose-dependent manner and the highest level of miR-155 was observed at 24 h after 100 ng/mL LPS treatment qPCR Pre-eclampsia [134]
  Mouse brain tissues Intraperitoneal injection of LPS 0.8 mg/kg single injection miR-155 expression level was increased by LPS in comparison to the control mice qPCR Neuroinflammation [125]
  Mouse tibiae Intraperitoneal injection of LPS 5 mg/kg once a week for 3 weeks The expression of miR-155 in the tibiae of LPS-treated mice was approximately 3.4-fold higher than that in vehicle treated ones qPCR Inflammatory bone loss [118]
  Mouse myocardium tissues Intraperitoneal injection of LPS 5 mg/kg single injection miR-155 expression level was markedly elevated in the myocardium as early as 5 h post-LPS injection and at least persisted to 24 h qPCR Sepsis-induced myocardial dysfunction [127]
  Mouse liver tissues Intraperitoneal injection of LPS 20 mg/kg single injection At 6 h and 12 h after LPS administration, the level of miR-155 in liver tissues showed about sixfold or sevenfold increase qPCR Septic liver injury [126]
  Mouse kidney tissues Intraperitoneal injection of LPS 20 mg/kg single injection Renal cortex miR-155 was highly induced after LPS treatment qPCR Sepsis-associated kidney injury [115]
  Mouse prostatic tissues Injection of LPS into the prostatic urinary tract 1 mg/mL single injection miR-155 expression levels were significantly increased in psoriasis tissues compared with normal tissues qPCR Chronic prostatitis [90]
  Mouse lung tissues Injection of LPS via the endotracheal intubation 1.25 mg/mL single injection miR-155 expression levels in mouse lungs were significantly upregulated and reached a peak at around 6 h after LPS stimulation qPCR Acute lung injury [128]
  Rat lung tissues Injection of LPS via the endotracheal intubation 10 mg/kg single injection miR-155 was significantly overexpressed in LPS-induced acute lung injury qPCR Acute lung injury [129]
  1. −: Not mentioned
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Cell Communication and Signaling

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