Osteoclast differentiation gene expression profiling reveals chemokine <scp>CCL4</scp> mediates <scp>RANKL</scp>‐induced osteoclast migration and invasion via <scp>PI3K</scp> pathway

Xuan, Wenhua; Feng, Xiaoke; Chen, Qian; Peng, Liuying; Shi, Yumeng; Xu, Lingxiao; Wang, Fang; Tan, Wenfeng

doi:10.1002/cbf.3260

Cited by 32 publications

(25 citation statements)

References 29 publications

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“…56 CCL4 has been found to be an important regulator for osteoclast migration indicating that it is a potential therapy target for bone resorptive diseases. 57 A study reported that CXCL10, CCL5 and CXCL8 chemokines were elevated in the plasma of patients with active RA similar to Th1 associated proinflammatory cytokines TNFα, and IL-6. 58 CXCL10 is primarily secreted by fibroblast-like synoviocytes and infiltrating macrophages in the synovium.…”

Section: Chemokines In Rheumatoid Arthritismentioning

confidence: 99%

<p>Role of Chemokines and Chemokine Receptors in Rheumatoid Arthritis</p>

Elemam¹,

Hannawi

Maghazachi³

2020

ITT

101

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Rheumatoid arthritis (RA) is one of the most prevalent autoimmune diseases and a prototypic inflammatory disease, affecting the small joints of the hands and feet. Chemokines and chemokine receptors play a critical role in RA pathogenesis via immune cells recruitment. Several chemokines and chemokine receptors are abundant in the peripheral blood and in the local inflamed joints of RA. Furthermore, synthetic and biologics disease modifying anti rheumatic drugs have been reported to affect chemokines expression. Thus, many studies have focused on targeting chemokines and chemokine receptors, where some have shown positive promising results. However, most of the chemokine blockers in human trials of RA treatment displayed some failures that can be attributed to several reasons in their structures and binding affinities. Nevertheless, targeting chemokines will continue to be under development, in order to improve their therapeutic potentials in RA and other autoimmune diseases. In this review we provide an up-to-date knowledge regarding the role of chemokines and chemokine receptors in RA with an emphasis on their activities on immune cells. We also discussed the effects of drugs targeting those molecules in RA. This knowledge might provide impetus for developing new therapeutic modalities to treat this chronic disease.

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Section: Chemokines In Rheumatoid Arthritismentioning

confidence: 99%

<p>Role of Chemokines and Chemokine Receptors in Rheumatoid Arthritis</p>

Elemam¹,

Hannawi

Maghazachi³

2020

ITT

101

View full text Add to dashboard Cite

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“…CX3CL1 derived from OBs enhances osteoclastogenesis by inducing the adhesion of OC precursors to the bone resorption site ( 79 ). A recent study demonstrated that CCL4 is as an important regulator of OC migration via induction of PI3K activation ( 80 ). Furthermore, CCL2 (MIP-1), CCL5 (RANTES), CCL7 (MCP-3), and CXCL12 (SDF-1) can also induce OC migration, resorption activity, adhesion, and survival ( 81 82 ).…”

Section: Osteoclastogenic Cytokines and Chemokinesmentioning

confidence: 99%

Regulation of Osteoclast Differentiation by Cytokine Networks

et al. 2018

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Cytokines play a pivotal role in maintaining bone homeostasis. Osteoclasts (OCs), the sole bone resorbing cells, are regulated by numerous cytokines. Macrophage colony-stimulating factor and receptor activator of NF-κB ligand play a central role in OC differentiation, which is also termed osteoclastogenesis. Osteoclastogenic cytokines, including tumor necrosis factor-α, IL-1, IL-6, IL-7, IL-8, IL-11, IL-15, IL-17, IL-23, and IL-34, promote OC differentiation, whereas anti-osteoclastogenic cytokines, including interferon (IFN)-α, IFN-β, IFN-γ, IL-3, IL-4, IL-10, IL-12, IL-27, and IL-33, downregulate OC differentiation. Therefore, dynamic regulation of osteoclastogenic and anti-osteoclastogenic cytokines is important in maintaining the balance between bone-resorbing OCs and bone-forming osteoblasts (OBs), which eventually affects bone integrity. This review outlines the osteoclastogenic and anti-osteoclastogenic properties of cytokines with regard to osteoimmunology, and summarizes our current understanding of the roles these cytokines play in osteoclastogenesis.

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“…Disruption of bone homeostasis is caused by increased bone resorption by osteoclasts rather than new bone formation by osteoblasts, and RANKL is a major pro-osteoclastogenic cytokine that mediates osteoclast differentiation ( Park et al., 2017 ; Ono and Nakashima, 2018 ). Thus, the inhibition of osteoclast formation, bone resorption and migration by inhibiting RANKL signaling and downstream pathways is an important target in the treatment of osteoporosis ( Zou et al., 2001 ; Xuan et al., 2017 ). In the present study, we evaluated the mechanism of CTU inhibition of osteoclast differentiation and migration in a RANKL-induced RAW 264.7 and BMM cell line.…”

Section: Discussionmentioning

confidence: 99%

“…In addition, osteoclast migration plays an important role in diseases associated with abnormal bone resorption such as rheumatoid arthritis and osteoporosis. In recent studies, chemokine CCL4 has been shown to mediate cell migration and bone invasion in RANKL-induced bone resorption ( Xuan et al., 2017 ). In this study, CTU downregulated the expression of transcription factors and genes involved in RANKL-induced osteoclast differentiation and migration.…”

Section: Discussionmentioning

confidence: 99%

Inhibitory Effect of Cudratrixanthone U on RANKL-Induced Osteoclast Differentiation and Function in Macrophages and BMM Cells

et al. 2020

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Cudratrixanthone U (CTU) is a prenylated xanthone compound isolated from Maclura tricuspidata Bureau (Moraceae). Prenylated xanthones have been reported to exhibit a variety of biological activities. However, the effects of prenylated xanthone on osteoclast differentiation and function are still unclear. Excessive bone resorption by osteoclasts is considered a major cause of diseases such as osteoporosis. Accordingly, suppression of excessive osteoclast formation and function is one of strategies for treating osteoclast related bone diseases. In this study, CTU inhibited osteoclast differentiation and function in RAW264.7 macrophages and BMM cells induced by receptor activator of nuclear factor-κB ligand (RANKL). CTU regulated the formation of TRAF6-TAK1 complex in RANKL-induced RAW264.7 macrophages and BMM cells. Osteoclast-specific genes including those encoding matrix metallopeptidase 9 (MMP-9), dendritic cell-specific transmembrane proteins (DC-STAMP), cathepsin K (CTSK) and chemokine CC motif ligand 4 (CCL4) play an important role in bone resorption and migration, and were effectively regulated by CTU. These results suggest that CTU is a potential therapeutic agent in osteoporosis.

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Osteoclast differentiation gene expression profiling reveals chemokine CCL4 mediates RANKL‐induced osteoclast migration and invasion via PI3K pathway

Cited by 32 publications

References 29 publications

<p>Role of Chemokines and Chemokine Receptors in Rheumatoid Arthritis</p>

<p>Role of Chemokines and Chemokine Receptors in Rheumatoid Arthritis</p>

Regulation of Osteoclast Differentiation by Cytokine Networks

Inhibitory Effect of Cudratrixanthone U on RANKL-Induced Osteoclast Differentiation and Function in Macrophages and BMM Cells

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