TRIM28/TIF1β and Fli-1 negatively regulate peroxynitrite generation via DUOX2 to decrease the shedding of membrane-bound fractalkine in human macrophages after exposure to substance P

Yamaguchi, Rui; Haraguchi, Misa; Yamaguchi, Reona; Sakamoto, Arisa; Narahara, Sayoko; Sugiuchi, Hiroyuki; Yamaguchi, Yasuo

doi:10.1016/j.cyto.2020.155180

Cited by 4 publications

(4 citation statements)

References 51 publications

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“…Indeed, a recent study in human macrophages subjected to substance P highlighted the role of DUOX2 in the production of the soluble extracellular form of CX3CL1 via the H 2 O 2 ‐dependent activation of the metalloprotease activity of ADAM10/17. 49 Similarly, DUOX1‐mediated oxidative activation of Src kinase and EGFR was shown to be critical for calpain‐2‐dependent IL‐33 secretion in airway ECs challenged with allergens. 50 Further studies will be required to elucidate the molecular mechanisms involved in DUOX2‐dependent regulation of selected cytokines and chemokines in virus‐infected ECs.…”

Section: Discussionmentioning

confidence: 99%

“…A possible alternative mechanism could be the regulation of cytokine trafficking. Indeed, a recent study in human macrophages subjected to substance P highlighted the role of DUOX2 in the production of the soluble extracellular form of CX3CL1 via the H 2 O 2 ‐dependent activation of the metalloprotease activity of ADAM10/17 49 . Similarly, DUOX1‐mediated oxidative activation of Src kinase and EGFR was shown to be critical for calpain‐2‐dependent IL‐33 secretion in airway ECs challenged with allergens 50 .…”

Section: Discussionmentioning

confidence: 99%

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DUOX2 regulates secreted factors in virus‐infected respiratory epithelial cells that contribute to neutrophil attraction and activation

et al. 2023

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

DUOX2 regulates secreted factors in virus‐infected respiratory epithelial cells that contribute to neutrophil attraction and activation

et al. 2023

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“…6 Stimulation of human monocytes with Fli-1 inhibitor CPT will significantly downregulate production of CXCL10 in the presence of IFNγ. 1 Moreover, for role of Fli-1 in macrophages, a study showed that Fli-1 inhibited production of peroxynitrite by interacting with Dual oxidase 2 (DUOX2), which will down-regulate the shedding of membranebound fractalkine in human macrophages in response to substance P. 7 Peritoneal macrophages from Fli-1 flox/flox LysMCre +/+ mice showed high expression of markers of alternative macrophage activation (CD163, FIZZ1 [resistin-like molecule alpha 1]), and haploinsufficient loss of Fli-1 strongly induced CXCL13 expression in murine peritoneal macrophages. 8,9 However, Fli-1 haploinsufficiency markedly inhibited CXCL6 expression in murine peritoneal macrophages in response to LPS, where Fli-1 bound to CXCL6 gene promoter in macrophages.…”

Section: Impact Of Fli-1 On Immune Cellsmentioning

confidence: 99%

Targeting Fli‐1 and chemokine axis CXCL10/CXCL13/CXCR3 in systemic lupus erythematosus and lupus nephritis

Zhu

2024

Int J of Rheum Dis

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Fli‐1 is a critical factor involved in hematopoietic stem cells, vascular endothelial cells apoptosis, and differentiation. Similarly, Fli‐1 regulates immune cell proliferation and differentiation, such as T cells, B cells, and monocytes. Regarding T/B cell dysfunction, SLE including LN is recognized to be associated with abnormal expression and function of Fli‐1. Moreover, three ligands of Fli‐1 including CXCL10 (C‐X‐C motif chemokine ligand 10), CXCR3 (C‐X‐C motif chemokine receptor 3), CXCL13 are widely discussed in SLE/LN. In this comprehensive review, we not only discussed Fli‐1 within SLE/LN pathogenesis, but also discussed the effects of CXCL10, CXCR3, and CXCL13 on SLE/LN development. Furthermore, we discussed how Fli‐1 regulates CXCL10, CXCR3, and CXCL13, and then involved in lupus development. It is possible that the Fli‐1 axis might be a potential target in SLE and LN.

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“…This makes us further hypothesize that SP/NK1R signaling is closely associated with fractalkine shedding to enhance soluble fractalkine levels. We recently reported that SP induces the shedding of membrane-bound fractalkine in human macrophages [20]. We also review the regulatory mechanism of activation of ADAMs by SP/ NK1R signaling.…”

Section: Introductionmentioning

confidence: 99%

The Role of Membrane-embedded DUOX2 on Ectodomain Shedding via G protein-coupled Receptor Signaling

2021

Journal of Cellular Signaling

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Protease-activated receptors (PARs) and the neurokinin 1 receptor (NK1R) belong to the G protein-coupled receptor (GPCR) family. In this review, we focus on the regulatory mechanism of ectodomain shedding by ADAM10/17 metalloprotease via GPCR signaling. PAR2 and NK1R induce membrane blebbing, resulting in phosphatidylserine externalization in the cellular membrane, which is required for ADAM10/17 metalloprotease activation. Membrane-embedded dual oxidase 2 (DUOX2) has NADPH oxidase and peroxidase domains. NADPH oxidase domain generates hydrogen peroxide (H 2 O 2 ), while the peroxidase domain produces peroxynitrite (ONOO − ) through the interaction of nitrogen oxide with superoxide. Both H 2 O 2 and peroxynitrite activate ADAM10/17 metalloproteases. PAR2 signaling activates ADAM10/17 by NADPH-mediated H 2 O 2 , leading to the transactivation of DUOX2/EGFR/TLR4 to synergistically upregulate IL-12p40 production after exposure to LPS. In contrast, nitric oxide (NO) synthesis is promoted by NK1R signaling, and DUOX2 generates ONOO-, preferentially activating ADAM10/17 metalloprotease. Ectodomain shedding of membrane-bound fractalkine is mediated by ADAM10/17. Substance P (SP)/NK1R signals enhance shedding of membrane-bound fractalkine, whereas small interfering RNA for DUOX2 further increases membrane-bound fractalkine but decreases soluble fractalkine compared with cells treated with SP alone. Considering the signaling pathway of TGFβ1 (an inhibitor of iNOS mRNA expression), silencing of RNA for TAK-1 upregulates membrane-bound fractalkine tripartite motif 28 (TRIM28)/transcriptional intermediary factor 1β (TIF1β) functions as an E3 ubiquitin ligase and specificity protein 1 negatively regulate TGFβ1 levels to upregulate the generation of peroxynitrite, leading to increased shedding of membrane-bound fractalkine via SP/NK1R signaling. DUOX2 plays a pivotal role for ectodomain shedding through ADAM10/17 activation by GPCR signaling.

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TRIM28/TIF1β and Fli-1 negatively regulate peroxynitrite generation via DUOX2 to decrease the shedding of membrane-bound fractalkine in human macrophages after exposure to substance P

Cited by 4 publications

References 51 publications

DUOX2 regulates secreted factors in virus‐infected respiratory epithelial cells that contribute to neutrophil attraction and activation

DUOX2 regulates secreted factors in virus‐infected respiratory epithelial cells that contribute to neutrophil attraction and activation

Targeting Fli‐1 and chemokine axis CXCL10/CXCL13/CXCR3 in systemic lupus erythematosus and lupus nephritis

The Role of Membrane-embedded DUOX2 on Ectodomain Shedding via G protein-coupled Receptor Signaling

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