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RGC-32 and diseases: the first 20 years

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Abstract

The response gene to complement (RGC)-32 acts as a cell cycle regulator and mediator of TGF-β effects. However, recent studies have revealed other functions for RGC-32 in diverse processes such as cellular migration, differentiation, and fibrosis. In addition to its induction by complement activation and the C5b-9 terminal complement complex, RGC-32 expression is also stimulated by growth factors, hormones, and cytokines. RGC-32 is induced by TGF-β through Smad3 and RhoA signaling and plays an important role in cell differentiation. In particular, RGC-32 is essential for the differentiation of Th17 cells. RGC-32−/− mice display an attenuated experimental autoimmune encephalomyelitis phenotype that is accompanied by decreased central nervous system inflammation and reductions in IL-17- and GM-CSF-producing CD4+ T cells. Accumulating evidence has drawn attention to the deregulated expression of RGC-32 in human cancers, atherogenesis, metabolic disorders, and autoimmune disease. Furthermore, RGC-32 is a potential therapeutic target in multiple sclerosis and other Th17-mediated autoimmune diseases. A better understanding of the mechanism(s) by which RGC-32 contributes to the pathogenesis of all these diseases will provide new insights into its therapeutic potential.

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Abbreviations

α-SMA:

alpha smooth muscle actin

AEC:

aortic endothelial cells

BATF:

Basic leucine zipper transcription factor

CDC2:

cell division cycle protein 2 homolog

EBV:

Epstein–Barr virus

EAE:

experimental autoimmune encephalomyelitis

ECM:

extracellular matrix

EMT:

epithelial to mesenchymal transition

HFD:

high-fat diet

ICAM-1:

intercellular adhesion molecules 1

IRF4:

interferon regulatory factor 4

KO:

knockout

MAPK:

mitogen-associated protein kinase

MMP:

matrix metalloproteinases

MS:

multiple sclerosis

PI3K:

phosphatidylinositol-3-kinase

PIGF:

placental growth factor

RGC-32:

response gene to complement 32

ROCK:

rho-associated coiled-coil-containing protein kinase

SLE:

systemic lupus erythematosus

SMC:

smooth muscle cells

VCAM-1:

vascular cell adhesion molecule 1

VEGF:

vascular endothelial growth factor

WT:

wild type

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Acknowledgments

We thank Dr. Deborah McClellan for editing this manuscript.

Funding

This work was supported in part by Veterans Administration Merit Award I01BX001458 (to H.R.).

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Authors and Affiliations

  1. Department of Internal Medicine, “Iuliu Hatieganu” University of Medicine and Pharmacy, Cluj-Napoca, Romania

    Sonia I. Vlaicu & Romeo Chira

  2. Department of Neurology, University of Maryland, School of Medicine, 655 W Baltimore St., BRB 12-033, Baltimore, MD, 21201, USA

    Sonia I. Vlaicu, Alexandru Tatomir, Freidrich Anselmo, Dallas Boodhoo & Horea Rus

  3. Department of Neurosciences, “Iuliu Hatieganu” University of Medicine and Pharmacy, Cluj-Napoca, Romania

    Alexandru Tatomir

  4. Department of Medicine, Division of Rheumatology and Immunology, University of Maryland, School of Medicine, Baltimore, MD, USA

    Violeta Rus

  5. Research Service, Veterans Administration Maryland Health Care System, Baltimore, MD, USA

    Horea Rus

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  1. Sonia I. Vlaicu
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Horea Rus has received a grant from TEVA Neuroscience (CNS-2014-174). All other authors declare that they have no conflict of interest.

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Vlaicu, S.I., Tatomir, A., Anselmo, F. et al. RGC-32 and diseases: the first 20 years. Immunol Res 67, 267–279 (2019). https://doi.org/10.1007/s12026-019-09080-0

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