Chemerin/chemR23 axis in inflammation onset and resolution

Mariani, Francesco; Roncucci, Luca

doi:10.1007/s00011-014-0792-7

Cited by 142 publications

(151 citation statements)

References 87 publications

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“…Similar data have been observed in vitro in squamous cancer cells, where PPL downregulation reduced cellular motility and Akt activation (19). Akt activation in Ppl -/-mice might also be due to the binding of chemerin to its main receptor ChemR23, whose activation leads to the upregulation of the phosphatidylinositol 3-kinase/ Akt signaling pathway and to downregulation of NF-κB (42).…”

Section: Discussionsupporting

confidence: 67%

Identification of periplakin as a major regulator of lung injury and repair in mice

Besnard¹,

Dagher²,

Madjer³

et al. 2018

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Section: Discussionsupporting

confidence: 67%

Identification of periplakin as a major regulator of lung injury and repair in mice

Besnard¹,

Dagher²,

Madjer³

et al. 2018

JCI Insight

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“…Adipocytokines are secreted by white adipose tissue and are thought to link obesity with the development of metabolic diseases (5). Many adipocytokines, including adiponectin, resistin and chemerin contribute to the development of insulin resistance and lowgrade inflammation (6,7). Adiponectin and resistin exert opposite effects on glucose metabolism: while adiponectin sensitises tissues to insulin, the latter promotes development of insulin resistance (8).…”

Section: Biochemical Assessmentmentioning

confidence: 99%

“…Adiponectin and resistin exert opposite effects on glucose metabolism: while adiponectin sensitises tissues to insulin, the latter promotes development of insulin resistance (8). Chemerin is also an adipocytokine implicated in the immune response with both pro and antiinflammatory properties (6). All these cytokines not only play roles in metabolism but also are involved in development of chronic inflammation (9).…”

Section: Biochemical Assessmentmentioning

confidence: 99%

Effects of secukinumab on serum adipocytokines: preliminary data

et al. 2017

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SUMMARYPsoriatic arthritis (PsA) is a chronic inflammatory disease that affects joints, connective tissues and the axial skeleton. Metabolic syndrome is an independent risk factor for psoriasis (Pso) development and is associated with more severe forms of Pso. Adipocytokines are secreted by white adipose tissue and are thought to link obesity with the development of metabolic and cardiovascular diseases. Secukinumab is a new monoclonal antibody with a different mechanism of action. This antibody selectively binds to and neutralizes interleukin-17 (IL-17) and it has shown efficacy in the treatment of PsA. The aim of this study was to evaluate the possible interferences of secukinumab on different adipocytokines. We enrolled 28 patients with PsA, classified with the CASPAR criteria. Serum samples were stored at baseline and then at the first, the third and the sixth month of therapy. Resistin, chemerin, adiponectin and C-reactive protein (CRP) were dosed. When tested globally, none of the adipokine tested showed any statistically significant variation. However, when the male group was tested, both resistin and chemerin at M6 showed a significant decrease from baseline. CRP did not show any variation at any time point. Our study demonstrated that treatment with secukinumab has little influence on the levels of adipokines tested within the first six months of treatment even though it might exert different influence between males and females from a metabolic perspective. Further studies with greater numbers of patients are needed to determine whether these preliminary results have clinical relevance.Key words: Psoriasis; psoriatic arthritis; secukinumab; adipokines; resistin; adiponectin; chemerin. Reumatismo, 2017; 69 (3): 105-110 n INTRODUCTION P soriasis (Pso) is a common chronic inflammatory disease involving the skin that can be associated with several comorbidities, one of which is psoriatic arthritis (PsA) (1). Psoriatic arthritis is a chronic, systemic inflammatory disease affecting peripheral joints, connective tissues, and the axial skeleton and is associated with psoriasis of the skin and nails (1). Patients with Pso and PsA share obesity (and related complications) and cardiovascular (CV) diseases. Chronic inflammation in Pso and PsA can partially explain the development of atherosclerosis and CV diseases, but also the concomitant alterations in the glucose metabolism (diabetes and insulin resistance) and lipids (dyslipidaemia) enhance this risk (2). Systemic inflammation induced by obesity and metabolic syndrome could exacerbate local inflammation, worsening both Pso and PsA (3). Indeed, increasing evidence is suggesting that metabolic syndrome is an independent risk factor for Pso development and is associated with more severe forms of Pso (3). Nowadays, adipose tissue is considered as an active endocrine and immune organ, producing various cytokines, named adipocytokines, and they link together inflammation and metabolic disorders (4). Adipocytokines, in cooperation with macrophages and T cells, ind...

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“…29 The differential role of chemerin/ChemR23 in the control of inflammation depends on the site of inflammation and the class of proteases predominating in the microenvironment. 30 Recent data demonstrate that in addition to regulating metabolic and inflammatory processes, chemerin may influence vascular function. Chemerin decreases nitric oxide (NO)-dependent cGMP signaling, thereby reducing vascular relaxation in rat aorta, an effect related to increased superoxide anion (O 2 − ·) generation.…”

Section: Hypertensionmentioning

confidence: 99%

Chemerin Regulates Crosstalk Between Adipocytes and Vascular Cells Through Nox

et al. 2015

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Adipocytes produce adipokines, including chemerin, a chemoattractant that mediates effects through its ChemR23 receptor. Chemerin has been linked to endothelial dysfunction and vascular injury in pathological conditions, such as obesity, diabetes mellitus, and hypertension. Molecular mechanisms underlying this are elusive. Here we assessed whether chemerin through redox-sensitive signaling influences molecular processes associated with vascular growth, apoptosis, and inflammation. Human microvascular endothelial cells and vascular smooth muscle cells were stimulated with chemerin (50 ng/mL). Chemerin increased generation of reactive oxygen species and phosphorylation of mitogen-activated protein kinases, effects that were inhibited by ML171, GKT137831 (Nox inhibitors), and N-acetylcysteine (reactive oxygen species scavenger). Chemerin increased mRNA expression of proinflammatory mediators in vascular cells and increased monocyte-to-endothelial cell attachment. In human vascular smooth muscle cells, chemerin induced phosphorylation of mitogen-activated protein kinases and stimulated proliferation (increased proliferating cell nuclear antigen expression [proliferation marker] and BrdU incorporation [proliferation assay]). Chemerin decreased phosphatidylinositol 3-kinase/protein kinase B activation and increased TUNEL-positive human vascular smooth muscle cells. In human microvascular endothelial cells, chemerin reduced endothelial nitric oxide synthase activity and nitric oxide production. Adipocyte-conditioned medium from obese/diabetic mice (db/db), which have elevated chemerin levels, increased reactive oxygen species generation in vascular smooth muscle cells, whereas adipocyte-conditioned medium from control mice had no effect. Chemerin actions were blocked by CCX 832, a ChemR23 inhibitor. Our data demonstrate that chemerin, through Nox activation and redox-sensitive mitogen-activated protein kinases signaling, exerts proapoptotic, proinflammatory, and proliferative effects in human vascular cells. These findings elucidate some molecular mechanisms through chemerin, which is increased in obesity, whereby adipocytes may influence vascular function. We identify chemerin as a novel vasoactive adipokine, which may be important in obesity-related vascular injury.

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Chemerin/chemR23 axis in inflammation onset and resolution

Cited by 142 publications

References 87 publications

Identification of periplakin as a major regulator of lung injury and repair in mice

Identification of periplakin as a major regulator of lung injury and repair in mice

Effects of secukinumab on serum adipocytokines: preliminary data

Chemerin Regulates Crosstalk Between Adipocytes and Vascular Cells Through Nox

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