An angiotensin receptor blocker suppresses monocyte chemoattractant protein 1 production from rheumatoid synovial fibroblasts: Comment on the article by Sagawa et al

Iikuni, Noriko; Okamoto, Hiroshi; Kasahara, Mika; Kamatani, Naoyuki

doi:10.1002/art.21431

Cited by 4 publications

(3 citation statements)

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“…The levels of MCP‐1/CCL2 correlate significantly with the levels of IL‐1β, IL‐6 and IL‐8/CXCL8 in culture supernatants of synovium from RA patients, and the expression of MCP‐1/CCL2 mRNA by cultured synovial cells is stimulated by IL‐1β and TNF‐α [20]. We recently found that angiotensin II activated nuclear factor‐κB in FLS to induce MCP‐1/CCL2 [21].…”

Section: Chemokinesmentioning

confidence: 99%

Molecular aspects of rheumatoid arthritis: chemokines in the joints of patients

et al. 2008

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Rheumatoid arthritis (RA) is a chronic symmetric polyarticular joint disease that primarily affects the small joints of the hands and feet. The inflammatory process is characterized by infiltration of inflammatory cells into the joints, leading to proliferation of synoviocytes and destruction of cartilage and bone. In RA synovial tissue, the infiltrating cells such as macrophages, T cells, B cells and dendritic cells play important role in the pathogenesis of RA. Migration of leukocytes into the synovium is a regulated multi‐step process, involving interactions between leukocytes and endothelial cells, cellular adhesion molecules, as well as chemokines and chemokine receptors. Chemokines are small, chemoattractant cytokines which play key roles in the accumulation of inflammatory cells at the site of inflammation. It is known that synovial tissue and synovial fluid from RA patients contain increased concentrations of several chemokines, such as monocyte chemoattractant protein‐4 (MCP‐4)/CCL13, pulmonary and activation‐regulated chemokine (PARC)/CCL18, monokine induced by interferon‐γ (Mig)/CXCL9, stromal cell‐derived factor 1 (SDF‐1)/CXCL12, monocyte chemotactic protein 1 (MCP‐1)/CCL2, macrophage inflammatory protein 1α (MIP‐1α)/CCL3, and Fractalkine/CXC3CL1. Therefore, chemokines and chemokine‐receptors are considered to be important molecules in RA pathology.

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Section: Chemokinesmentioning

confidence: 99%

Molecular aspects of rheumatoid arthritis: chemokines in the joints of patients

et al. 2008

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“…We found that angiotensin II is also an inducer of NF‐κB activation in FLS. We have shown that angiotensin II activated NF‐κB in synovial cells to induce the monocyte chemoattractant protein‐1 and that the angiotensin receptor blocker inhibited this activation [13].…”

Section: Nuclear Factor‐κbmentioning

confidence: 99%

Molecular aspects of rheumatoid arthritis: role of transcription factors

et al. 2008

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Rheumatoid arthritis is a multifactorial disease characterized by chronic inflammation of the joints. Both genetic and environmental factors are involved in the pathogenesis leading to joint destruction and ultimately disability. In the inflamed RA joint the synovium is highly infiltrated by CD4+ T cells, B cells and macrophages, and the intimal lining becomes hyperplastic owing to the increased number of macrophage‐like and fibroblast‐like synoviocytes. This hyperplastic intimal synovial lining forms an aggressive front, called pannus, which invades cartilage and bone structures, leading to the destruction and compromised function of affected joints. This process is mediated by a number of cytokines (tumor necrosis factor‐α, interleukin‐1, interleukin‐6, interleukin‐17 interferon‐γ, etc.), chemokines (monocyte chemoattractant protein‐1, monocyte chemoattractant protein‐4 CCL18, etc.), cell adhesion molecules (intercellular adhesion molecule‐1, vascular cell adhesion molecule‐1, etc.) and matrix metalloproteinases. Expression of these molecules is controlled at the transcription level and activation of a limited number of transcription factors is involved in this process.

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“…After nuclear translocation, NF-κB binds to its specific binding site on DNA to activate gene expression in association with transcription machinery, such as coactivators. NF-κB is a transcription factor that regulates the gene expression of inflammatory cytokines such as interleukin-6, monocyte chemoattractant protein 1, AT1 receptor, and platelet-derived growth factor-beta (PDGF-B) in several cells [ 5 , 6 ]. Therefore, in concert with the immunological attack on the virus, the elevation of angiotensin II by SARS-CoV2 infection could induce NF-κB activation in bronchial epithelial cells and vascular endothelial cells, leading to the recruitment of inflammatory cells and enhanced cytokine/chemokine and PDGF-B expression.…”

mentioning

confidence: 99%