FAM19A5, a brain-specific chemokine, inhibits RANKL-induced osteoclast formation through formyl peptide receptor 2

Park, Min Young; Kim, Hyung Sik; Lee, Mingyu; Park, Byung‐Hyun; Lee, Ha Young; Cho, Eun Bee; Seong, Jae Young; Bae, Yoe Sik

doi:10.1038/s41598-017-15586-0

Cited by 38 publications

(44 citation statements)

References 41 publications

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“…,34 Accordingly, we have been suggested that WKYMVm, another FPR2 agonist, also suppresses osteoclastogenesis under both normal and inflammatory condition. In this study, we demonstrated that WKYMVm negatively regulates osteoclast…”

mentioning

confidence: 99%

The protective effect of WKYMVm peptide on inflammatory osteolysis through regulating NF‐κB and CD9/gp130/STAT3 signalling pathway

Chen

et al. 2019

J Cellular Molecular Medi

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The balance between bone formation and bone resorption is closely related to bone homeostasis. Osteoclasts, originating from the monocyte/macrophage lineage, are the only cell type possessing bone resorption ability. Osteoclast overactivity is thought to be the major reason underlying osteoclast‐related osteolytic problems, such as Paget's disease, aseptic loosening of prostheses and inflammatory osteolysis; therefore, disruption of osteoclastogenesis is considered a crucial treatment option for these issues. WKYMVm, a synthetic peptide, which is a potent FPR2 agonist, exerts an immunoregulatory effect. This peptide inhibits the production of inflammatory cytokines, such as (IL)‐1β and TNF‐α, thus regulating inflammation. However, there are only few reports on the role of WKYMVm and FPR2 in osteoclast cytology. In the current study, we found that WKYMVm negatively regulates RANKL‐ and lipopolysaccharide (LPS)‐induced osteoclast differentiation and maturation in vitro and alleviates LPS‐induced osteolysis in animal models. WKYMVm down‐regulated the expression of osteoclast marker genes and resorption activity. Furthermore, WKYMVm inhibited osteoclastogenesis directly through reducing the phosphorylation of STAT3 and NF‐kB and indirectly through the CD9/gp130/STAT3 pathway. In conclusion, our findings demonstrated the potential medicinal value of WKYMVm for the treatment of inflammatory osteolysis.

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mentioning

confidence: 99%

The protective effect of WKYMVm peptide on inflammatory osteolysis through regulating NF‐κB and CD9/gp130/STAT3 signalling pathway

Chen

et al. 2019

J Cellular Molecular Medi

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“…Wang et al showed FAM19A5 inhibits the vascular smooth muscle cells proliferation and ameliorates neointima formation in the injured rat carotid arteries (8). Although several studies addressed contribution of FAM19A5 to neurological disorders (19)(20)(21)(22)(23), existing data on a relevant association of FAM19A5 and cardiac and metabolic disorders are very limited (8,9). To our knowledge, this is the first clinical observation pointing to the association of FAM19A5 with the pathogenesis of NAFLD.…”

Section: Introductionmentioning

confidence: 80%

“…Several studies have shown association of FAM19A5 gene with neurological and/or psychiatric diseases (19-22, 25, 26). FAM19A5 has been linked to in ammation, differentiation and cognition (19,21,23,26,27). But few studies have addressed the role of FAM19A5 in cardiometabolic disorders.…”

Section: Discussionmentioning

confidence: 99%

Circulating levels of FAM19A5 are inversely associated with subclinical atherosclerosis in non-alcoholic fatty liver disease

Yari

Shabani

Karami

et al. 2020

Preprint

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Background: Family with sequence similarity 19 (chemokine (C-C motif)-like) member A5 (FAM19A5) is a newly identified adipokine. There is a limited number of studies linking FAM19A5 to metabolic disorders. In the current study, we aimed to explore if FAM19A5 is associated with nonalcoholic fatty liver disease (NAFLD). We also sought to determine the possibility of FAM19A5 association with subclinical atherosclerosis in NAFLD patients. Methods: A total of 69 subjects including 37 NAFLD and 32 control subjects were included in this cross-sectional study. Plasma concentration of FAM19A5 was measured with the ELISA method. Carotid artery intima-media thickness (cIMT) was assessed by the ultrasonography.Results: Plasma concentration of FAM19A5 in patients with NAFLD was significantly lower in NAFLD patients than controls. Moreover, we observed significant negative correlations between plasma level of FAM19A5 and body mass index (BMI), visceral fat, alanine amino transferase (ALT), aspartate amino transferase (AST), liver stiffness (LS), and cIMT. Following stepwise multiple linear regression analysis, ALT and cIMT were the only determinants of FAM19A5 level. Conclusions: This is the first report to describe association of circulating FAM19A5 levels with NAFLD. Our findings provide further evidence showing relation of FAM19A5 with the risk of atherosclerosis. However, more studies are necessary to unravel the contribution of lower FAM19A5 levels to the NAFLD pathogenesis and the higher risk of atherosclerosis in these patients.

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“…A intronic variant of FAM19A5 (family with sequence similarity 19 member A5) gene on 22q13.32 was also associated with an increased risk of pancreatic cancer (rs5768709). This gene encodes a TAFA protein expressed predominately in brain and may function as brain-specific chemokines or neurokines 198 . Prior to the ChinaPC study, there is no implication of PRLHR or FAM19A5 in the risk of pancreatic cancer and thus their susceptibility role is currently unknown.…”

Section: Common Low-risk Susceptibility Locimentioning

confidence: 99%

Inherited pancreatic cancer

Chen¹,

Roberts²,

Klein³

2017

Chin. Clin. Oncol.

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Pancreatic cancers arise through a series of genetic events both inherited and acquired. Inherited genetic changes, both high penetrance and low penetrance, are an important component of pancreatic cancer risk, and may be used to characterize populations who will benefit from early detection. Furthermore, pancreatic cancer patients with inherited mutations may be particularly sensitive to certain targeted agents, providing an opportunity to personalized treatment. Family history of pancreatic cancer is one of the strongest risk factors for the disease, and is associated with an increased risk of caners at other sites, including but not limited to breast, ovarian and colorectal cancer. The goal of this chapter is to discuss the importance of family history of pancreatic cancer, and the known genes that account for a portion of the familial clustering of pancreatic cancer.

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FAM19A5, a brain-specific chemokine, inhibits RANKL-induced osteoclast formation through formyl peptide receptor 2

Cited by 38 publications

References 41 publications

The protective effect of WKYMVm peptide on inflammatory osteolysis through regulating NF‐κB and CD9/gp130/STAT3 signalling pathway

The protective effect of WKYMVm peptide on inflammatory osteolysis through regulating NF‐κB and CD9/gp130/STAT3 signalling pathway

Circulating levels of FAM19A5 are inversely associated with subclinical atherosclerosis in non-alcoholic fatty liver disease

Inherited pancreatic cancer

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