Dual role of Response gene to complement-32 in multiple sclerosis

Tegla, Cosmin; Cudrici, Cornelia; Azimzadeh, Philippe; Singh, Anil; Trippe, Richard; Khan, Ali S.; Chen, Hegang; Andrian-Albescu, Maria; Royal, Walter; Bever, Christopher T.; Rus, Violeta; Rus, Horea

doi:10.1016/j.yexmp.2012.09.005

Cited by 39 publications

(65 citation statements)

References 38 publications

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“…RGC-32 plays a role in the immune response which has been determined [29]. Recent studies reported that levels of RGC-32 mRNA in PBMCs were significantly higher in patients with stable SM as compared with patients who had a relapse (active disease) [8] and the RGC-32 protein expressions in macrophages and T cells were significantly increased in the colonic mucosa of patients with inflammatory bowel disease [9]. Our study demonstrates that not only the plasma RGC-32 levels but intracellular RGC-32 expression of CD4 + T cells were also significantly increased in DCM patients.…”

Section: Discussionmentioning

confidence: 99%

“…For transient knockdown of RGC-32, siRNA against human RGC-32 (Santa Cruz Biotech, Santa Cruz, CA, USA) was nucleofected into the resting PBMCs using Nucleofector kit for human primary T cells (Amaxa, Gaithersberg, MD, USA) according to the manufacturer's instructions. A scrambled siRNA was used as control [8]. The efficiency of transfection for RGC-32 was confirmed by Western blotting.…”

Section: Plasmid Sirna and Pbmcs Transfectionmentioning

confidence: 99%

“…In RGC-32-deficient mice, demonstrated that RGC-32 -/-CD4 + T cells exhibited enhanced proliferation, IL-2 production, and Akt phosphorylation as compared with RGC-32 +/+ CD4 + T cells, suggesting a down-regulatory role of RGC-32 under Th0 conditions [7]. Tegla and Vlaicu et al reported increased expression of RGC-32 protein in macrophages, T cells, and astrocytes in the brain of patients with multiple sclerosis (MS) and in the colonic mucosa of patients with inflammatory bowel disease [8,9].…”

Section: Introductionmentioning

confidence: 99%

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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%

Section: Plasmid Sirna and Pbmcs Transfectionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

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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“…Consistent with the presence of RGC-32 in M2 macrophages, this protein has been detected in CD68 1 macrophages in multiple sclerosis plaques, and the expression of this cell marker is regulated by TGF-b. 21 Therefore, RGC-32 expression marks a wider range of alternatively activated macrophages.…”

Section: Cd14mentioning

confidence: 99%

“…[16][17][18][19] Interestingly, RGC-32 is abnormally expressed in the peripheral blood mononuclear cells of patients with hyper-immunoglobulin E syndrome and multiple sclerosis. 20,21 Little is known about the role of RGC-32 in immunity. In the present study, we show that RGC-32 is expressed at high levels in M2 macrophages and TAMs and that tumors induce RGC-32 expression in an M-CSF-and/or IL-4-dependent manner.…”

Section: Introductionmentioning

confidence: 99%

Response gene to complement 32 (RGC-32) expression on M2-polarized and tumor-associated macrophages is M-CSF-dependent and enhanced by tumor-derived IL-4

et al. 2014

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Response gene to complement 32 (RGC-32) is a cell cycle regulator involved in the proliferation, differentiation and migration of cells and has also been implicated in angiogenesis. Here we show that RGC-32 expression in macrophages is induced by IL-4 and reduced by LPS, indicating a link between RGC-32 expression and M2 polarization. We demonstrated that the increased expression of RGC-32 is characteristic of alternatively activated macrophages, in which this protein suppresses the production of pro-inflammatory cytokine IL-6 and promotes the production of the anti-inflammatory mediator TGF-b. Consistent with in vitro data, tumor-associated macrophages (TAMs) express high levels of RGC-32, and this expression is induced by tumor-derived ascitic fluid in an M-CSF-and/or IL-4-dependent manner. Collectively, these results establish RGC-32 as a marker for M2 macrophage polarization and indicate that this protein is a potential target for cancer immunotherapy, targeting tumor-associated macrophages.

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