ATF3 Inhibits Tenascin-C-induced Foam Cell Formation in LPS-Stimulated THP-1 Macrophages by Suppressing TLR-4

Luo, Hong; Wang, Jing; Qiao, Chenhui; Zhang, Xin; Zhang, Weihua; Ma, Ning

doi:10.5551/jat.28415

Cited by 13 publications

(7 citation statements)

References 27 publications

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“…32 In addition, ATF3 inhibits tenascin C-induced foam cell formation by suppressing TLR4 in LPS-stimulated THP-1 macrophages. 33 These data clearly show that ATF3 plays an atheroprotective role in macrophages.…”

Section: Role Of Atf3 In Mediating the Anti-inflammatory Effect Ofmentioning

confidence: 69%

Activating transcription factor 3 in immune response and metabolic regulation

Jadhav

Zhang

2017

Liver Research

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Activating transcription factor 3 (ATF3) is a member of the ATF/cAMP-response element binding protein (CREB) family of transcription factors. In response to stress stimuli, ATF3 forms dimers to activate or repress gene expression. Further, ATF3 modulates the immune response, atherogenesis, cell cycle, apoptosis, and glucose homeostasis. Recent studies have shown that ATF3 may also be involved in pathogenesis of other diseases. However, more studies are needed to determine the role of ATF3 in metabolic regulation.

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Section: Role Of Atf3 In Mediating the Anti-inflammatory Effect Ofmentioning

confidence: 69%

Activating transcription factor 3 in immune response and metabolic regulation

Jadhav

Zhang

2017

Liver Research

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“…The negative regulator of NF-κB gene promoters, ATF3, was already greatly induced by MAP at 1 hpi (5.1-fold) and also for the entire infection period (Supplementary Table 4). ATF3 is the transcriptional inhibitor of tenascin-C (TNC) (43). Supporting the TNC downregulation effect of ATF3, TNC was one of the most downregulated genes by MAP infection, being reduced 148 times at 1 hpi in MAP-infected JD(-) macrophages ( Table 1).…”

Section: Inflammatory Processesmentioning

confidence: 82%

Transcriptome Profiling of Bovine Macrophages Infected by Mycobacterium avium spp. paratuberculosis Depicts Foam Cell and Innate Immune Tolerance Phenotypes

et al. 2020

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Mycobacterium avium spp. paratuberculosis (MAP) is the causative agent of Johne's disease (JD), also known as paratuberculosis, in ruminants. The mechanisms of JD pathogenesis are not fully understood, but it is known that MAP subverts the host immune system by using macrophages as its primary reservoir. MAP infection in macrophages is often studied in healthy cows or experimentally infected calves, but reports on macrophages from naturally infected cows are lacking. In our study, primary monocyte-derived macrophages (MDMs) from cows diagnosed as positive (+) or negative (-) for JD were challenged in vitro with live MAP. Analysis using nextgeneration RNA sequencing revealed that macrophages from JD(+) cows did not present a definite pattern of response to MAP infection. Interestingly, a considerable number of genes, up to 1436, were differentially expressed in JD(-) macrophages. The signatures of the infection time course of 1, 4, 8, and 24 h revealed differential expression of ARG2,

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“…Quantitatively, NCoR1/2 were enriched at sites of ATF3 binding relative to ATF2 ( Extended Data Figs. 4k – n ), providing a plausible mechanism for the reported immunosuppressive functions of ATF3 23 – 26 , including ATF3-dependent repression of Tlr4 25 , 27 . Conversely, the depletion of NCoR1/2 at ATF2/HDAC3 binding sites contributes to the physiological basis for DA-independent gene activation.…”

mentioning

confidence: 95%

Dichotomous engagement of HDAC3 activity governs inflammatory responses

Nguyen

Adlanmérini

Hauck

et al. 2020

Nature

112

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Histone deacetylase 3 (HDAC3) is unique among the HDAC superfamily of chromatin modifiers that silence transcription through enzymatic modification of histones because interaction with nuclear receptor corepressors (NCoR1/2) is required for engagement of its catalytic activity 1 – 3 . However, loss of HDAC3 also represses transcription 4 – 8 . Here we report that, during lipopolysaccharide (LPS) activation of macrophages, recruitment of HDAC3 to ATF2-bound sites without NCoR1/2 non-canonically activates inflammatory gene expression. By contrast, HDAC3 deacetylase activity is selectively engaged at ATF3-bound sites that suppress toll-like receptor (TLR) signaling. Deletion of HDAC3 in macrophages safeguards mice from lethal exposure to LPS, but this protection is not conferred by genetic or pharmacological abolition of HDAC3 catalytic activity. Thus, HDAC3 is a dichotomous transcriptional activator and repressor whose non-canonical deacetylase-independent functions are vital for the innate immune system.

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ATF3 Inhibits Tenascin-C-induced Foam Cell Formation in LPS-Stimulated THP-1 Macrophages by Suppressing TLR-4

Cited by 13 publications

References 27 publications

Activating transcription factor 3 in immune response and metabolic regulation

Activating transcription factor 3 in immune response and metabolic regulation

Transcriptome Profiling of Bovine Macrophages Infected by Mycobacterium avium spp. paratuberculosis Depicts Foam Cell and Innate Immune Tolerance Phenotypes

Dichotomous engagement of HDAC3 activity governs inflammatory responses

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