Inhibition of regulator of G protein signaling 10, aggravates rheumatoid arthritis progression by promoting NF-κB signaling pathway

Ren, Jie; Wei, Wei; Tan, Liangyu; Yang, Qin; Lu, Qi; Ding, Hong; Yue, Yuan; Tian, Ye; Hao, Liang; Wang, Min; Li, Jinle

doi:10.1016/j.molimm.2021.03.024

Cited by 11 publications

(14 citation statements)

References 40 publications

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“…S-Y Ma et al reported that KCNMA1 inhibits the apoptosis of ovarian cancer cells, which serves as a biomarker for patients with ovarian cancer 42 . GPCR mediates various physiologic and pathologic processes, including cancer, aging, inflammation, and diabetes dysfunctions [43][44][45][46][47][48][49][50][51][52][53][54][55][56][57][58][59][60][61][62] . The GPCR regulator β-arr1 increases liver fibrosis via Snail signaling, and β-arr1 may be a therapeutic target for liver fibrosis 63 .…”

Section: Discussionmentioning

confidence: 99%

Identification of transcriptional landscapes and functions of the inhibition of ARHGEF2 in hepatocellular carcinoma cells

Zhang

Chung

2022

Preprint

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The RHO guanine exchange factor ARHGEF2 has exchange activity toward RHOA, which is essential for the development of cancers such as liver cancer. However, the potential functions and mechanisms of ARHGEF2 in the progression of liver cancer are largely unknown. In this study, we identified the transcriptional landscapes of hepatocellular carcinoma cells treated with ARHGEF2 shRNAs. The gene enrichment assays such as KEGG and GO were used to further analyze the potential signaling pathways. Moreover, the PPI network and Reactome map were used to further identify the biological processes. The results showed that Alzheimer's disease disease (AD) and Cushing syndrome (CS) are the major signaling pathways involved in the ARHGEF2-shRNAs treated hepatocellular carcinoma cells. We identified the top ten interactive genes including ICAM1, APOE, LDLR, NAT10, HSPA1A, EDN1, CACNA1C, KCNMA1, SNAI1, and ELN. Our study may provide novel mechanisms for the treatment of liver cancer by inhibiting ARHGEF2.

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Section: Discussionmentioning

confidence: 99%

Identification of transcriptional landscapes and functions of the inhibition of ARHGEF2 in hepatocellular carcinoma cells

Zhang

Chung

2022

Preprint

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“…More specifically, RGS10 suppresses NF- κ B activation and the expression of inflammatory genes such as TNF-α, interleukins, COX-2 and iNOS in multiple types of (resident and recruited) macrophages ( 18 – 20 , 23 , 24 ). Several studies have investigated the role of RGS10 in inflammation-associated diseases, such Parkinson’s disease ( 23 ), multiple sclerosis ( 33 ), thioglycolate-induced peritonitis ( 19 ), osteopetrosis ( 34 – 36 ), cardiac hypertrophy ( 37 ), chemoresistant ovarian cancer ( 38 – 41 ), platelets aggregation and thrombogenesis ( 42 – 46 ), obesity and related metabolic syndromes ( 47 ), rheumatoid arthritis ( 48 ), and colitis-related neurologic dysfunction ( 49 ).…”

Section: Discussionmentioning

confidence: 99%

RGS10 Reduces Lethal Influenza Infection and Associated Lung Inflammation in Mice

et al. 2021

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Seasonal influenza epidemics represent a significant global health threat. The exacerbated immune response triggered by respiratory influenza virus infection causes severe pulmonary damage and contributes to substantial morbidity and mortality. Regulator of G-protein signaling 10 (RGS10) belongs to the RGS protein family that act as GTPase activating proteins for heterotrimeric G proteins to terminate signaling pathways downstream of G protein-coupled receptors. While RGS10 is highly expressed in immune cells, in particular monocytes and macrophages, where it has strong anti-inflammatory effects, its physiological role in the respiratory immune system has not been explored yet. Here, we show that Rgs10 negatively modulates lung immune and inflammatory responses associated with severe influenza H1N1 virus respiratory infection in a mouse model. In response to influenza A virus challenge, mice lacking RGS10 experience enhanced weight loss and lung viral titers, higher mortality and significantly faster disease onset. Deficiency of Rgs10 upregulates the levels of several proinflammatory cytokines and chemokines and increases myeloid leukocyte accumulation in the infected lung, markedly neutrophils, monocytes, and inflammatory monocytes, which is associated with more pronounced lung damage. Consistent with this, influenza-infected Rgs10-deficent lungs contain more neutrophil extracellular traps and exhibit higher neutrophil elastase activities than wild-type lungs. Overall, these findings propose a novel, in vivo role for RGS10 in the respiratory immune system controlling myeloid leukocyte infiltration, viral clearance and associated clinical symptoms following lethal influenza challenge. RGS10 also holds promise as a new, potential therapeutic target for respiratory infections.

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“…RGS proteins are widely associated with bone development and remodeling under physiological and pathological conditions (10,20,21). Osteoblasts and osteoclasts are the two main constituents that can be affected by RGS proteins (Figure 1).…”

Section: Role Of Rgs Proteins In Bonementioning

confidence: 99%

“…Moreover, the impacts of RGS proteins on a variety of GPCR signaling pathways have been determined in those animal models (9,18). Up to now, the RGS family members have been divided into nine subfamilies including RZ (RGS17, 19,20), R4 (RGS1-5, 8, 13, 16, 18, 21), R7 (RGS6, 7, 9, 11), R12 (RGS10, 12,14), RA (AXIN, AXIN2), GEF (p115-RhoGEF, PDZ-RhoGEF, LARG), GRK (GRK1-7), SNX (SNX13, 14, 25), and others (RGS22, D-AKAP2) (19). Some RGS proteins and their signaling pathways have been discovered to regulate skeletal formation/remodeling, and the changes in these RGS proteins leads to various bone diseases in human.…”

Section: Introductionmentioning

confidence: 99%

Effect of Regulator of G Protein Signaling Proteins on Bone

Yuan

Yang

2022

Front. Endocrinol.

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Regulator of G protein signaling (RGS) proteins are critical negative molecules of G protein-coupled receptor (GPCR) signaling, which mediates a variety of biological processes in bone homeostasis and diseases. The RGS proteins are divided into nine subfamilies with a conserved RGS domain which plays an important role in regulating the GTPase activity. Mutations of some RGS proteins change bone development and/or metabolism, causing osteopathy. In this review, we summarize the recent findings of RGS proteins in regulating osteoblasts, chondrocytes, and osteoclasts. We also highlight the impacts of RGS on bone development, bone remodeling, and bone-related diseases. Those studies demonstrate that RGS proteins might be potential drug targets for bone diseases.

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Inhibition of regulator of G protein signaling 10, aggravates rheumatoid arthritis progression by promoting NF-κB signaling pathway

Cited by 11 publications

References 40 publications

Identification of transcriptional landscapes and functions of the inhibition of ARHGEF2 in hepatocellular carcinoma cells

Identification of transcriptional landscapes and functions of the inhibition of ARHGEF2 in hepatocellular carcinoma cells

RGS10 Reduces Lethal Influenza Infection and Associated Lung Inflammation in Mice

Effect of Regulator of G Protein Signaling Proteins on Bone

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