NLRP12 negatively regulates EtOH-induced liver macrophage activation via NF-κB pathway and mediates hepatocyte apoptosis in alcoholic liver injury

Zhang, Yafei; Bu, Fang-tian; Yin, Na-Na; wang, Ao; You, Hongmei; Jia, Wen-qian; Huang, Cheng; Li, Jun

doi:10.1016/j.intimp.2020.106968

Cited by 20 publications

(7 citation statements)

References 46 publications

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“…of some key transcription factors, such as nuclear factor kappa B (NF-jB), Kr€ uppel-like factor (KLF)4 and peroxisome proliferator-activated receptor c [3][4][5]. Many studies report that M1 macrophages show an anti-tumorigenic phenotype by promoting the inflammation.…”

Section: Introductionmentioning

confidence: 99%

“…Macrophages can be simply divided into two extreme subtypes: classical polarization (M1 macrophages) and alternative polarization (M2 macrophages) [2]. Macrophage polarization is the selective expression of related marker genes and the activation of some key transcription factors, such as nuclear factor kappa B (NF‐κB), Krüppel‐like factor (KLF)4 and peroxisome proliferator‐activated receptor γ [3–5]. Many studies report that M1 macrophages show an anti‐tumorigenic phenotype by promoting the inflammation.…”

Section: Introductionmentioning

confidence: 99%

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SENP1‐KLF4 signalling regulates LPS‐induced macrophage M1 polarization

Wang

Xiong

et al. 2022

The FEBS Journal

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Macrophages are very important immune cells and play critical roles in tumour immunity. Macrophage subtypes can be divided into classical polarization (M1 macrophages) and alternative polarization (M2 macrophages) under different microenvironments. Krüppel‐like factor 4 (KLF4) is an essential transcription factor for macrophage polarization. Our previous study has shown that KLF4 SUMOylation plays an important role in macrophage M2 polarization. In the present study, small ubiquitin‐like modifier (SUMO) specific peptidase (SENP)1 was identified as a specific protease for KLF4 de‐SUMOylation, with the SENP1‐KLF4 axis playing a vital role in M1 macrophage polarization by affecting the nuclear factor kappa B signalling pathway. Additionally, the activity of tumour cells was weakened by KLF4 SUMOylation deficient macrophages. Hence, the SENP1‐KLF4 axis is considered to play a crucial role in regulating lipopolysaccharide‐induced macrophage M1 polarization, thereby affecting the activity of tumour cells. Therefore, the SENP1‐KLF4 axis has therapeutic potential as a target in cancer therapy.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

SENP1‐KLF4 signalling regulates LPS‐induced macrophage M1 polarization

Wang

Xiong

et al. 2022

The FEBS Journal

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“…Apoptotic cell death is a mechanism by which cells function normally by eliminating harmful or severely damaged cells ( Ko et al, 2020 ; Shojaie et al, 2020 ). However, excessive hepatocyte apoptotic death rather leads to hepatic dysfunction, leading to acute liver injury ( Wang et al, 2019 ; Zhang et al, 2020 ).…”

Section: Introductionmentioning

confidence: 99%

Treadmill exercise ameliorates ethanol with lipopolysaccharide and carbon tetrachloride-mediated liver injury in mice

Kim¹,

Ko²,

Jin³

et al. 2022

J Exerc Rehabil

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We reported that application of ethanol with lipopolysaccharide (LPS) and carbon tetrachloride (CCl4) enhanced alanine aminotransferase (ALT) and aspartate aminotransferase (AST) level. In the current experiment, the protective effect of treadmill running on liver injury caused by ethanol with LPS and CCl4 in mice was studied. Liver injury severity was determined by measuring ALT and AST level in the blood. Terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling (TUNEL) staining, immunohistochemistry for caspase-3, and Western blotting for Bcl-2-associated X protein (Bax) and B-cell lymphoma 2 (Bcl-2) were performed to indicate hepatocyte apoptosis. In addition, to understand the mechanism, 5’-adenosine monophosphate-activated protein kinase (AMPK) phosphorylation was studied by Western blotting. Treadmill exercise ameliorated ethanol with LPS and CCl4-mediated elevation of ALT and AST level. Treadmill exercise suppressed ethanol with LPS and CCl4-mediated elevation of the TUNEL-positive cell number and cleaved caspase-3 expression. Treadmill exercise suppressed ethanol with LPS and CCl4-mediated elevation of Bax expression and increased Bcl-2 expression suppressed by application of ethanol with LPS and CCl4. Treadmill exercise enhanced AMPK phosphorylation which was suppressed by application of ethanol with LPS and CCl4. Treadmill exercise has the effect of reducing liver damage caused by alcohol and or drug addiction.

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“…The action of apoptosis is to keep cells functioning normally by eliminating harmful or severely damaged cells ( Ko et al, 2020a ; Shojaie et al, 2020 ). However, excessive hepatocellular death has the potential to cause liver dysfunction, causing to ALI ( Wang et al, 2019 ; Zhang et al, 2020 ).…”

Section: Introductionmentioning

confidence: 99%

Polydeoxyribonucleotide ameliorates alcoholic liver injury though suppressing phosphatidylinositol 3-kinase/protein kinase B signaling pathway in mice

Cho¹,

Ko²,

Jin³

et al. 2022

J Exerc Rehabil

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Polydeoxyribonucleotide (PDRN), which is adenosine A<sub>2A</sub> receptor agonist, facilitates healing and inhibits inflammation and apoptosis. The effect of PDRN on alcoholic liver injury (ALI) was evaluated focusing on the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt) signaling pathway. The mice were given daily oral administration of 50% ethanol at a dose of 4 g/kg during 8 weeks. After 4 weeks of alcohol intake, 200 μL of normal saline containing 8-mg/kg PDRN was intraperitoneally administered 3 times a week for 4 weeks. To determine whether the action of PDRN occurs through the adenosine A<sub>2A</sub> receptor, 8-mg/kg 3,7-dimethyl-1-propargylxanthine (DMPX) with PDRN was treated. The concentration of aspartate aminotransferase (AST) and alanine aminotransferase (ALT) was detected. For liver histopathological score, hematoxylin and eosin staining was conducted. Enzyme-linked immunoassay was used to measure cyclic adenosine-3′,5′-monophosphate (cAMP) concentration. PI3K and Akt expression was determined using Western blot analysis. In the results, PDRN treatment suppressed AST and ALT level in serum and liver tissue, and improved damaged liver tissue and decreased histological score. PDRN application inhibited the expression of phosphorylated PI3K/Akt signaling pathway. The increasing effect of PDRN on cAMP level ats as a mechanism for ALI treatment. Co-treatment of DMPX with PDRN did not reduce apoptosis, causing no improvement in liver function. As a result of this experiment, PDRN has the potential to be selected as a therapeutic agent for ALI.

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NLRP12 negatively regulates EtOH-induced liver macrophage activation via NF-κB pathway and mediates hepatocyte apoptosis in alcoholic liver injury

Cited by 20 publications

References 46 publications

SENP1‐KLF4 signalling regulates LPS‐induced macrophage M1 polarization

SENP1‐KLF4 signalling regulates LPS‐induced macrophage M1 polarization

Treadmill exercise ameliorates ethanol with lipopolysaccharide and carbon tetrachloride-mediated liver injury in mice

Polydeoxyribonucleotide ameliorates alcoholic liver injury though suppressing phosphatidylinositol 3-kinase/protein kinase B signaling pathway in mice

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