Chemerin induces endothelial cell inflammation: activation of nuclear factor-kappa beta and monocyte-endothelial adhesion

Dimitriadis, Georgios K.; Kaur, Jasbinder; Adya, Raghu; Miras, Alexander D.; Mattu, Harman S.; Hattersley, John; Kaltsas, Gregory; Tan, Bee K.; Randeva, Harpal S.

doi:10.18632/oncotarget.24659

Cited by 56 publications

(40 citation statements)

References 36 publications

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“…33 When activated by stimulators like physiological stresses, HG or lipopolysaccharide, it could induce the production of inflammatory factors. 35 In the present study, we also showed that phosphorylation of p38 MAKP could be induced by chemerin. 35 In the present study, we also showed that phosphorylation of p38 MAKP could be induced by chemerin.…”

Section: Discussionsupporting

confidence: 75%

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Chemerin/ChemR23 axis promotes inflammation of glomerular endothelial cells in diabetic nephropathy

Shang

Wang

Zhang

et al. 2019

J Cellular Molecular Medi

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Diabetic nephropathy (DN) is characterized by inflammation of renal tissue. Glomerular endothelial cells (GEnCs) play an important role in inflammation and protein leakage in urine in DN patients. Chemerin and its receptor ChemR23 are inducers of inflammation. The aim of this study was to investigate the function of chemerin/ChemR23 in GEnCs of DN patients. Immunohistochemical staining and qRT‐PCR were used to measure the expression of chemerin, ChemR23 and inflammatory factors in renal tissues of DN patients. Db/db mice were used as animal model. ChemR23 of DN mice was knocked down by injecting LV3‐shRNA into tail vein. Inflammation, physiological and pathological changes in each group was measured. GEnCs were cultured as an in vitro model to study potential signalling pathways. Results showed that expression of chemerin, ChemR23 and inflammatory factors increased in DN patients and mice. LV3‐shRNA alleviated renal damage and inflammation in DN mice. GEnCs stimulated by glucose showed increased chemerin, ChemR23 and inflammatory factors and decreased endothelial marker CD31. Both LV3‐shRNA and SB203580 (p38 MAPK inhibitor) attenuated chemerin‐induced inflammation and injury in GEnCs. Taken together, chemerin/ChemR23 axis played an important role in endothelial injury and inflammation in DN via the p38 MAPK signalling pathway. Suppression of ChemR23 alleviated DN damage.

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Section: Discussionsupporting

confidence: 75%

“…34 In human endothelial cells, chemerin was reported to induce activation of the p38 MAPK pathway in a dose-dependent manner. 35 In the present study, we also showed that phosphorylation of p38 MAKP could be induced by chemerin. SB203580 is a widely used inhibitor of the p38 MAPK pathway.…”

Section: Serum Chemerin Level Was Closely Related With Renal Functionsupporting

confidence: 75%

Chemerin/ChemR23 axis promotes inflammation of glomerular endothelial cells in diabetic nephropathy

Shang

Wang

Zhang

et al. 2019

J Cellular Molecular Medi

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“…These proteins exist in most immune cells and are involved in both physiological and pathophysiological processes. Previous research demonstrated that chemerin effects on monocyte-endothelial adhesion via the MAPK and PI3K/Akt pathways [45]. In the present study, we observed that chemerin induced the phosphorylation of ERK MAPK, and p38 MAPK in HUVECs.…”

Section: Discussionsupporting

confidence: 71%

Chemerin Induced byTreponema pallidumPredicted Membrane Protein Tp0965 Mediates Endothelial Dysfunction via Activating MAPK Signaling Pathway

Zhang

Yang

Wang

2018

Preprint

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24Chemerin, a chemoattractant protein, is involved in endothelial dysfunction and 25 vascular inflammation in pathological conditions. In a recent study, we observed the 26 upregulation of chemerin in endothelial cells following in vitro treatment with T. 27 pallidum. Here, we investigated the role of chemerin in endothelial cells dysfunction 28 induced by the T. pallidum predicted membrane protein Tp0965. Following 29 stimulation of human umbilical vein endothelial cells (HUVECs) with Tp0965, 30 chemerin and its ChemR23 receptor were up-regulated, companied with elevated 31 expression of TLR2. Furthermore, chemerin from HUVECs activated endothelial cells 32 via chemerin/ChemR23 signaling in an autocrine/paracrine manner, characterized by 33 upregulated expression of ICAM-1, E-selectin and MMP-2. Activation of endothelial 34 cells depended on the MAPK signaling pathway. In addition, Tp0965-induced 35 chemerin promoted monocytes migration to endothelial cells, also via 36 chemerin/ChemR23 pathway. The RhoA/ROCK signaling pathway was also involved 37 in monocytes migration in response to chemerin/ChemR23. Our results highlight the 38 role of Tp0965-induced chemerin in endothelial cells dysfunction, which contributes to 39 the immunopathogenesis of vascular inflammation of syphilis.40 Author summary 41 Treponema pallidum is the spirochete of syphilis, which causes a chronic system 42 inflammation. Endothelium damage caused by this bacterium is the key step in the 43 systemic dissemination and pathophysiology of syphilis, particularly cardiovascular 44 syphilis and neurosyphilis. In this study, we show a novel molecular mechanism of 3 45 endothelium damage induce by Treponema pallidum predicted membrane protein 46 Tp0965. Chemerin is a recently identified adipocytokine and chemoattractant protein 47 with a crucial role in endothelial dysfunction and vascular inflammation in pathological 48 conditions. Our data show that Tp0965 up-regulated the expression of chemerin and its 49 ChemR23 receptor by endothelial cells in vitro. Furthermore, chemerin from HUVECs 50 activated endothelial cells via chemerin/ChemR23 signaling in an autocrine/paracrine 51 manner and depended on the MAPK signaling pathway. In addition, Tp0965-induced 52 chemerin promoted monocytes migration to endothelial cells, also via 53 chemerin/ChemR23 pathway. The RhoA/ROCK signaling pathway was also involved 54 in monocytes migration in response to chemerin/ChemR23. These findings contribute 55 to the immunopathogenesis of vascular inflammation of syphilis. 56 57 Introduction 58 Treponema pallidum subsp. pallidum (T. pallidum) is the spirochete of syphilis, a 59 sexually transmitted infection that remains an important public health problem around 60 the world [1]. Infection by this bacterium causes a chronic system inflammation, and if 61 untreated can seriously and irreversibly damage the nervous and cardiovascular system.62 Cardiovascular syphilis is associated with multiple clinical syndromes, of which aortic 63 aneurysms, aortic insufficiency,...

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“…In patients with CAD, circulating levels of chemerin also correlate with the severity of CAD [ 129 , 130 , 131 , 132 ]. Some studies carried out in HUVECs have shown that chemerin participates in endothelial inflammation by inducing nuclear factor-κB (NF-κB), which is a key player in vascular inflammation, atherosclerosis development, and its pathological complications in atherothrombotic diseases [ 133 , 134 ] and the monocyte–endothelial adhesion [ 135 ]. In human VSMCs, chemerin has pro-apoptotic, pro-inflammatory, and proliferative effects that are mediated by nicotinamide adenine dinucleotide phosphate oxidase (Nox) activation and redox-sensitive mitogen-activated protein kinases signalling [ 136 ].…”

Section: Role Of Some Adipokines In Inflammatory Processes Associamentioning

confidence: 99%

Adipokines and Inflammation: Focus on Cardiovascular Diseases

Feijóo‐Bandín

Aragón-Herrera

Moraña-Fernández

et al. 2020

IJMS

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It is well established that adipose tissue, apart from its energy storage function, acts as an endocrine organ that produces and secretes a number of bioactive substances, including hormones commonly known as adipokines. Obesity is a major risk factor for the development of cardiovascular diseases, mainly due to a low grade of inflammation and the excessive fat accumulation produced in this state. The adipose tissue dysfunction in obesity leads to an aberrant release of adipokines, some of them with direct cardiovascular and inflammatory regulatory functions. Inflammation is a common link between obesity and cardiovascular diseases, so this review will summarise the role of the main adipokines implicated in the regulation of the inflammatory processes occurring under the scenario of cardiovascular diseases.

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Chemerin induces endothelial cell inflammation: activation of nuclear factor-kappa beta and monocyte-endothelial adhesion

Cited by 56 publications

References 36 publications

Chemerin/ChemR23 axis promotes inflammation of glomerular endothelial cells in diabetic nephropathy

Chemerin/ChemR23 axis promotes inflammation of glomerular endothelial cells in diabetic nephropathy

Chemerin Induced byTreponema pallidumPredicted Membrane Protein Tp0965 Mediates Endothelial Dysfunction via Activating MAPK Signaling Pathway

Adipokines and Inflammation: Focus on Cardiovascular Diseases

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