Chemokines in idiopathic inflammatory myopathies

Paepe, Boél De; Creus, Kim K.; Bleecker, Jan De

doi:10.2741/2866

Cited by 43 publications

(35 citation statements)

References 49 publications

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“…CXCL9 and CXCL10 messenger RNAs are significantly elevated in IBM muscle compared with controls [19 ].…”

Section: A-chemokinesmentioning

confidence: 95%

“…Earlier reports localize CXCL9 to the CD8 þ T-cells of IBM and CXCL10 to the CD4 þ , CD68 þ and CD8 þ cells of the different IIMs [19 ]. CXCL9 is widely expressed on the surface of myofibers of IBM, where it colocalizes with MHC-I.…”

Section: A-chemokinesmentioning

confidence: 98%

“…The vast majority of T-cells in muscle tissues are CXCR3 þ [19 ], a chemokine receptor associated with the Th1 lineage. Two cytokines with strong Th1 association, namely IFN-g and TNF-a, are upregulated in dermatomyositis, polymyositis and IBM.…”

Section: Th1 Immune Response In Idiopathic Inflammatory Myopathiesmentioning

confidence: 99%

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Role of cytokines and chemokines in idiopathic inflammatory myopathies

Paepe

Creus

Bleecker

2009

Current Opinion in Rheumatology

117

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“…CXCL9 and CXCL10 messenger RNAs are significantly elevated in IBM muscle compared with controls [19 ].…”

Section: A-chemokinesmentioning

confidence: 95%

Section: A-chemokinesmentioning

confidence: 98%

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Role of cytokines and chemokines in idiopathic inflammatory myopathies

Paepe

Creus

Bleecker

2009

Current Opinion in Rheumatology

117

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“…CCL2 (MCP-1) is a chemotactic cytokine (8 kDa), which binds to CCR2 G-protein-coupled receptors to regulate macrophage recruitment during normal processes such as wound healing [6–13], and during inflammatory diseases such as rheumatoid arthritis [14, 15]. CCL2 is overexpressed in breast cancer tumors [16–18].…”

Section: Introductionmentioning

confidence: 99%

The CCL2 chemokine is a negative regulator of autophagy and necrosis in luminal B breast cancer cells

Fang

Yao

Jokar

et al. 2015

Breast Cancer Res Treat

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Luminal A and B breast cancers are the most prevalent forms of breast cancer diagnosed in women. Compared to luminal A breast cancer patients, patients with luminal B breast cancers experience increased disease recurrence and lower overall survival. The mechanisms that regulate the luminal B subtype remain poorly understood. The chemokine CCL2 is overexpressed in breast cancer, correlating with poor patient prognosis. The purpose of this study was to determine the role of CCL2 expression in luminal B breast cancer cells. Breast tissues, MMTV-PyVmT and MMTV-Neu transgenic mammary tumors forming luminal B-like lesions, were immunostained for CCL2 expression. To determine the role of CCL2 in breast cancer cells, CCL2 gene expression was silenced in mammary tumor tissues and cells using TAT cell-penetrating peptides non-covalently cross linked to siRNAs (Ca-TAT/siRNA). CCL2 expression was examined by ELISA and flow cytometry. Cell growth and survival were analyzed by flow cytometry, immunocytochemistry, and fluorescence microscopy. CCL2 expression was significantly increased in luminal B breast tumors, MMTV-PyVmT and MMTV-Neu mammary tumors, compared or normal breast tissue or luminal A breast tumors. Ca-TAT delivery of CCL2 siRNAs significantly reduced CCL2 expression in PyVmT mammary tumors, and decreased cell proliferation and survival. CCL2 gene silencing in PyVmT carcinoma cells or BT474 luminal B breast cancer cells decreased cell growth and viability associated with increased necrosis and autophagy. CCL2 expression is overexpressed in luminal B breast cancer cells and is important for regulating cell growth and survival by inhibiting necrosis and autophagy.

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“…In addition to its roles in the physiological events described above, SDF-1/CXCR4 has been implicated in inflammatory diseases (19), development and metastasis of cancers (20,21), and atherosclerosis (22). Therefore, SDF-1/CXCR4 has become a potential therapeutic target for treatment of a variety of diseases such as human immunodeficiency virus infection, cancer metastasis, leukemia, rheumatoid arthritis, and stroke (23,24).…”

mentioning

confidence: 99%

Inhibition of Gluconeogenesis in Primary Hepatocytes by Stromal Cell-derived Factor-1 (SDF-1) through a c-Src/Akt-dependent Signaling Pathway

Liu

Wen

Han

et al. 2008

Journal of Biological Chemistry

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Hepatic gluconeogenesis is elevated in diabetes and a major contributor to hyperglycemia. Stromal cell-derived factor-1 (SDF-1) is a chemokine and an activator of Akt. In this study, we tested the hypothesis that SDF-1 suppresses hepatic gluconeogenesis through Akt. Our results from isolated primary hepatocytes show that SDF-1␣ and SDF-1␤ inhibited glucose production via gluconeogenesis and reduced transcript levels of key gluconeogenic genes glucose-6-phosphatase (G6Pase) and phosphoenolpyruvate carboxykinase (PEPCK). Additionally, SDF-1␣ and SDF-1␤ both inhibited activation of the PEPCK promoter. In examining the mechanism by which SDF-1 inhibits gluconeogenesis, we found that SDF-1 promoted phosphorylation of Akt, FoxO1, and c-Src, but did not activate insulin receptor substrate-1-like insulin. Blockade of Akt activation by LY294002, FoxO1 translocation by constitutively nuclear FoxO1 mutant, or c-Src activation by the chemical inhibitor PP2, respectively, blunted SDF-1 suppression of gluconeogenesis. Finally, our results show that knocking down the level of SDF-1 receptor CXCR4 mRNA blocked SDF-1 suppression of gluconeogenesis. Together, our results demonstrate that SDF-1 is capable of inhibiting gluconeogenesis in primary hepatocytes through a signaling pathway distinct from the insulin signaling.

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Chemokines in idiopathic inflammatory myopathies

Cited by 43 publications

References 49 publications

Role of cytokines and chemokines in idiopathic inflammatory myopathies

Role of cytokines and chemokines in idiopathic inflammatory myopathies

The CCL2 chemokine is a negative regulator of autophagy and necrosis in luminal B breast cancer cells

Inhibition of Gluconeogenesis in Primary Hepatocytes by Stromal Cell-derived Factor-1 (SDF-1) through a c-Src/Akt-dependent Signaling Pathway

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