Response Gene to Complement 32 Protein Promotes Macrophage Phagocytosis via Activation of Protein Kinase C Pathway

Tang, Rui; Gui, Zhang; Chen, Shiyou

doi:10.1074/jbc.m114.566653

Cited by 35 publications

(40 citation statements)

References 40 publications

(38 reference statements)

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“…It is determined that the RGC-32 is expressed in PBMCs, lymphocytes, macrophages [8,43]. To further examine the effect of RGC-32 on the frequencies of Treg and Th17 cells, we conducted the overexpression or downregulation of RGC-32 in PBMCs from patients with DCM, and found the expression of RGC-32 was in direct correlation with the frequencies of Treg and Th17 cells.…”

Section: Discussionmentioning

confidence: 99%

Response Gene to Complement-32 Promotes the Imbalance of Treg/Th17 in Patients with Dilated Cardiomyopathy

Li¹,

Zhou²,

Tang³

et al. 2017

Cell Physiol Biochem

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Background/Aims: The imbalance of Treg/Th17 cells plays important role in the pathogenesis of dilated cardiomyopathy (DCM). Response gene to complement (RGC)-32 is a cell cycle regulator that plays an important role in cell proliferation. We evaluated whether the upregulation of RGC-32 was implicated in the homeostasis of Treg/Th17 cells in DCM. Methods:The levels of plasma RGC-32, IL-17 and TGF-β1, and the frequencies of circulating CD4 + RGC-32 + T cells, Th17 and Treg cells in patients with DCM were determined by Cytokinespecific sandwich ELISA and the flow cytometer (FCM), respectively. Results: A significant elevation of plasma RGC-32 in patients with DCM compared with healthy control (HC) subjects was observed. This upregulation was associated with an increase in frequency of Th17 and a decrease in frequency of Treg cells. To further assessed the role of RGC-32, we investigated the effects of RGC-32 up-or down-regulation on frequencies of Th17 and Treg cells in peripheral blood mononuclear cells (PBMCs) from subjects. Importantly, overexpression of RGC-32 was accompanied by an augmentation of Th17 and a reduction of Treg expression. Conclusion: In summary, our study demonstrated the up-regulation of RGC-32 contributed to the imbalance of Treg/Th17 cells in patients with DCM.

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Section: Discussionmentioning

confidence: 99%

Response Gene to Complement-32 Promotes the Imbalance of Treg/Th17 in Patients with Dilated Cardiomyopathy

Li¹,

Zhou²,

Tang³

et al. 2017

Cell Physiol Biochem

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“…RGC-32 is localized in the cytoplasm and translocates to the nucleus upon upregulation by complement activation, growth factors, and cytokines (6, 7). A membrane associated form was also described in macrophages (3). …”

mentioning

confidence: 91%

“…RGC-32 mRNA and protein expression was detected in primary and secondary lymphoid organs of normal mice (4, 12). Among innate immune cells, murine macrophages express a membrane-associated form that enhances phagocytosis (3). In adaptive immune cells, we recently reported that RGC-32 is upregulated in TCR-stimulated mouse CD4 + T cells (12).…”

mentioning

confidence: 99%

RGC-32 Promotes Th17 Cell Differentiation and Enhances Experimental Autoimmune Encephalomyelitis

Rus

Nguyen

Tatomir

et al. 2017

The Journal of Immunology

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Th17 cells play a critical role in autoimmune diseases, including multiple sclerosis and its animal model, experimental autoimmune encephalomyelitis. Response gene to complement (RGC)-32 is a cell cycle regulator and a downstream target of TGF-β that mediates its profibrotic activity. In this study, we report that RGC-32 is preferentially upregulated during Th17 cell differentiation. RGC-32−/− mice have normal Th1, Th2, and regulatory T cell differentiation but show defective Th17 differentiation in vitro. The impaired Th17 differentiation is associated with defects in IFN regulatory factor 4, B cell–activating transcription factor, retinoic acid–related orphan receptor γt, and SMAD2 activation. In vivo, RGC-32−/− mice display an attenuated experimental autoimmune encephalomyelitis phenotype accompanied by decreased CNS inflammation and reduced frequency of IL-17– and GM-CSF–producing CD4+ T cells. Collectively, our results identify RGC-32 as a novel regulator of Th17 cell differentiation in vitro and in vivo and suggest that RGC-32 is a potential therapeutic target in multiple sclerosis and other Th17-mediated autoimmune diseases.

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“…Response gene to complement 32 (RGC‐32) primarily acts as a cell cycle regulator involved in cell proliferation and differentiation, but reports regarding its function in inflammatory responses have been inconsistent. RGC‐32 is important for M2 macrophage polarization and phagocytic activity, and inhibits development of the M1 macrophage . The M1/M2 macrophage polarization scheme parallels the T‐helper (Th)1/Th2 paradigm, whereby the M1 phenotype produces pro‐inflammatory cytokines and the M2 phenotype is more of an anti‐inflammatory nature .…”

mentioning

confidence: 99%

Decreased expression of response gene to complement 32 in psoriasis and its association with reduced M2 macrophage polarization

Kim

Jang

Lee

et al. 2019

The Journal of Dermatology

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Response Gene to Complement 32 Protein Promotes Macrophage Phagocytosis via Activation of Protein Kinase C Pathway

Cited by 35 publications

References 40 publications

Response Gene to Complement-32 Promotes the Imbalance of Treg/Th17 in Patients with Dilated Cardiomyopathy

Response Gene to Complement-32 Promotes the Imbalance of Treg/Th17 in Patients with Dilated Cardiomyopathy

RGC-32 Promotes Th17 Cell Differentiation and Enhances Experimental Autoimmune Encephalomyelitis

Decreased expression of response gene to complement 32 in psoriasis and its association with reduced M2 macrophage polarization

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