Myeloid Sirtuin 6 Deficiency Causes Insulin Resistance in High-Fat Diet–Fed Mice by Eliciting Macrophage Polarization Toward an M1 Phenotype

Lee, Youngyi; Ka, Sun-O; Cha, Hye-Na; Chae, Yuna; Kim, Mi-Kyung; Park, Soyoung; Bae, Eun Ju; Park, Byung‐Hyun

doi:10.2337/db16-1446

Cited by 97 publications

(94 citation statements)

References 41 publications

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“…And our data also were in line with published reports that most actions of ANG II were primarily carried out by AT 1 R signaling . Additionally, inhibition of Erk1/2, p38, or Stat3 could also obviously ameliorate the cardiac injury, which cannot completely owe to prevent M1 polarization; as all these inhibitors are not specific for macrophage polarization, more and more data indicated that macrophage polarization was associated with Erk1/2, p38, or Stat3; therefore, our data suggested that to prevent the macrophage polarization, the EAM development could be ameliorated.…”

Section: Discussionsupporting

confidence: 91%

ANG II facilitated CD11+Ly6Chi cells reprogramming into M1-like macrophage through Erk1/2 or p38-Stat3 pathway and involved in EAM

Shao

et al. 2018

Journal of Leukocyte Biology

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Macrophage, a highly plastic population, is widely distributed. Macrophage functions are settled and acquired polarization programs in response to microenvironmental signals and involved in many inflammatory disorders, such as experimental autoimmune myocarditis (EAM). Phenotypic and functional changes in macrophage are considered as an important determinant of disease progression and/or regression. Angiotensin II (ANG II), as a powerful proinflammatory factor, plays critical roles in inflammatory diseases and macrophage recruitment. It remains unclear whether ANG II contributed to the functional skewing of cardiac infiltrated monocytes/macrophage and involved in EAM development. Therefore, the present work was to address the above questions. Our data showed that ANG II contributed to CD11b Ly6C (CD11b Ly6G Ly6C ) cells reprogramming into M1-like macrophage through Erk1/2 or p38/Stat3 pathway and the reprogramming M1-like cells promoted Th17 cells expansion; abrogation of ANG II-AT R axis significantly ameliorated cardiac injury. The present work first demonstrated a novel immune regulation role of ANG II; ANG II, as a powerful immune factor, promoted CD11b Ly6C inflammatory cells reprogramming into M1-like macrophage and involved in inflammatory disorders development; our results also indicated that ANG II may be a potential therapeutic target for inflammatory diseases.

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Section: Discussionsupporting

confidence: 91%

ANG II facilitated CD11+Ly6Chi cells reprogramming into M1-like macrophage through Erk1/2 or p38-Stat3 pathway and involved in EAM

Shao

et al. 2018

Journal of Leukocyte Biology

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“…Furthermore, NDTR-treated M0 macrophages showed the reduced expression of CD23 with increased expression of CD163 and CD206 (Figure 4D and 4E). Although these results indicate that NDTR-treated macrophages did not exhibit the classical patterns of M1/M2 markers, recent studies suggest that the surface marker expression patterns of macrophages polarized toward M1 by exogenous compounds do not always follow those for classical M1 macrophages (Lee et al, 2017; Xu et al, 2016; Zhang et al, 2018). Therefore, we defined the phenotype of NDTR-treated macrophages as M1-like macrophages based on the expression of important functional markers of M1 macrophages, such as iNOS, TNF-α, and IL-12, in NDTR-treated macrophages.…”

Section: Resultscontrasting

confidence: 62%

Neutrophil-derived extracellular vesicles: proinflammatory trails and anti-inflammatory microvesicles

Youn

Shrestha

et al. 2019

Preprint

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SUMMARYExtracellular vesicles (EVs) are membrane-derived vesicles that mediate intercellular communications. Neutrophils produce different subtypes of EVs during inflammatory responses. Neutrophil-derived trails (NDTRs) are generated by neutrophils migrating toward inflammatory foci, whereas neutrophil-derived microvesicles (NDMVs) are thought to be generated by neutrophils that have arrived at the inflammatory foci. However, the physical and functional characteristics of neutrophil-derived EVs are incompletely understood. In this study, we investigated the similarities and differences between neutrophil-derived EV subtypes. Neutrophil-derived EVs shared similar characteristics regarding stimulators, generation mechanisms, and surface marker expression. Both neutrophil-derived EV subtypes exhibited similar functions, such as direct bactericidal activity and induction of monocyte chemotaxis via MCP-1. However, NDTR generation was dependent on the integrin signaling, while NDMV generation was dependent on the PI3K pathway. The CD16 expression level differentiated the neutrophil-derived EV subtypes. Interestingly, both subtypes showed different patterns of miRNA expression and were easily phagocytosed by monocytes. NDTRs induced M1 macrophage polarization, whereas NDMVs induced M2 macrophage polarization. Moreover, NDTRs but not NDMVs exerted protective effects against sepsis-induced lethality in a murine sepsis model and pathological changes in a murine chronic colitis model. These results suggest a new insight into neutrophil-derived EV subtypes: proinflammatory NDTRs and anti-inflammatory NDMVs.Key pointsNeutrophil-derived trails are proinflammatory extracellular vesicles that induce M1 macrophage polarization and protect against inflammationNeutrophil-derived microvesicles are anti-inflammatory extracellular vesicles that induce M2 macrophage polarization

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“…Maternal obesity is afflicted with many maternal obstetric complications in the offspring including high blood pressure, obesity, gestational diabetes and increased perinatal morbidity . Several factors are involved in the progression of IR induced by HFD including inflammation, excessive ROS, abnormal immune response, lipotoxicity and altered glycosylation . Recently, an important role for protein quality control, particularly autophagy, has been depicted in the maintenance of metabolic homeostasis .…”

Section: Discussionmentioning

confidence: 99%

“…23 Several factors are involved in the progression of IR induced by HFD including inflammation, excessive ROS, abnormal immune response, lipotoxicity and altered glycosylation. 1,[24][25][26][27][28] Recently, an important role for protein quality control, particularly autophagy, has been depicted in the maintenance of metabolic homeostasis. 29 However, the mechanism underlying IR is far from clarified.…”

Section: Discussionmentioning

confidence: 99%

P53/PANK1/miR‐107 signalling pathway spans the gap between metabolic reprogramming and insulin resistance induced by high‐fat diet

Yang

Zhang

Wang

et al. 2020

J Cellular Molecular Medi

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High‐fat diet (HFD) leads to obesity, type II diabetes mellitus (T2DM) and increases the coincidence of cardiovascular diseases and cancer. Insulin resistance (IR) is considered as the ‘common soil’ of those diseases. Furthermore, people on HFD showed restrained glycolysis and enhanced fatty acid oxidation, which is the so‐called metabolic reprogramming. However, the relationship between metabolic reprogramming and IR induced by HFD is still unclear. Here, we demonstrate that PANK1 and miR‐107 were up‐regulated in the liver tissue of mice on HFD for 16 weeks and involved in metabolic reprogramming induced by palmitate acid (PA) incubation. Importantly, miR‐107 within an intron of PANK1 gene facilitated IR by targeting caveolin‐1 in AML12 cells upon PA incubation. Moreover, we identify that HFD enhanced P53 expression, and activation of P53 with nutlin‐3a induced PANK1 and miR‐107 expression simultaneously in transcriptional level, leading to metabolic reprogramming and IR, respectively. Consistently, inhibition of P53 with pifithrin‐α hydrobromide ameliorated PA‐induced metabolic reprogramming and IR. Thus, our results revealing a new mechanism by which P53 regulate metabolism. In addition, the results distinguished the different roles of PANK1 and its intron miR‐107 in metabolic regulation, which will provide more accurate intervention targets for the treatment of metabolic diseases.

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Myeloid Sirtuin 6 Deficiency Causes Insulin Resistance in High-Fat Diet–Fed Mice by Eliciting Macrophage Polarization Toward an M1 Phenotype

Cited by 97 publications

References 41 publications

ANG II facilitated CD11+Ly6Chi cells reprogramming into M1-like macrophage through Erk1/2 or p38-Stat3 pathway and involved in EAM

ANG II facilitated CD11+Ly6Chi cells reprogramming into M1-like macrophage through Erk1/2 or p38-Stat3 pathway and involved in EAM

Neutrophil-derived extracellular vesicles: proinflammatory trails and anti-inflammatory microvesicles

P53/PANK1/miR‐107 signalling pathway spans the gap between metabolic reprogramming and insulin resistance induced by high‐fat diet

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