Globular C1q receptor (p33) binds and stabilizes pro-inflammatory MCP-1: a novel mechanism for regulation of MCP-1 production and function

Anders, Emma; Nebel, Daniel; Westman, Johannes; Herwald, Heiko; Nilsson, Bengt‐Olof; Svensson, Daniel

doi:10.1042/bcj20170857

Cited by 11 publications

(15 citation statements)

References 35 publications

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“…Anders et al. ( 16 ) found that the globular C1q receptor (p33), a binding partner of C1q in the complement system, could stabilize CCL2 protein. In vitro studies have revealed high-affinity binding between CCL2 protein and p33, and recombinant p33 greatly enhanced CCL2 persistence and the migration capacity of THP-1 monocytes.…”

Section: Regulation Of Ccl2 Productionmentioning

confidence: 99%

“…In recent years, many non-canonical factors have been reported to directly bind to the cis-element of the CCL2 gene or protein independent of classical pathways. Anders et al (16) found that the globular C1q receptor (p33), a binding partner of C1q in the complement system, could stabilize CCL2 protein. In vitro studies have revealed high-affinity binding between CCL2 protein and p33, and recombinant p33 greatly enhanced CCL2 persistence and the migration capacity of THP-1 monocytes.…”

Section: Regulation Of Ccl2 Productionmentioning

confidence: 99%

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CCL2: An Important Mediator Between Tumor Cells and Host Cells in Tumor Microenvironment

et al. 2021

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Tumor microenvironment (TME) formation is a major cause of immunosuppression. The TME consists of a considerable number of macrophages and stromal cells that have been identified in multiple tumor types. CCL2 is the strongest chemoattractant involved in macrophage recruitment and a powerful initiator of inflammation. Evidence indicates that CCL2 can attract other host cells in the TME and direct their differentiation in cooperation with other cytokines. Overall, CCL2 has an unfavorable effect on prognosis in tumor patients because of the accumulation of immunosuppressive cell subtypes. However, there is also evidence demonstrating that CCL2 enhances the anti-tumor capability of specific cell types such as inflammatory monocytes and neutrophils. The inflammation state of the tumor seems to have a bi-lateral role in tumor progression. Here, we review works focusing on the interactions between cancer cells and host cells, and on the biological role of CCL2 in these processes.

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Section: Regulation Of Ccl2 Productionmentioning

confidence: 99%

Section: Regulation Of Ccl2 Productionmentioning

confidence: 99%

CCL2: An Important Mediator Between Tumor Cells and Host Cells in Tumor Microenvironment

et al. 2021

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“…Previous studies in peripheral cell types suggested its role in the regulation of oxidative phosphorylation, and also the regulation of mitochondrial gene expression either as a chaperone or as a transcription factor 17,24,32 . Among the many previously suggested functions of C1qbp, these mitochondrial functions but not immunosignalling of surface C1qbp 6,8,58 and cytosolic/nuclear mRNA chaperone functions 17,18 are likely based on its subcellular distribution in brain cells.…”

Section: Discussionmentioning

confidence: 96%

“…C1qbp (gC1qR) has been implicated in the modulation of the immune response to pathogens 5 . Different mechanisms have been proposed including the pro-inflammatory role of C1qbp (gC1qR) by promoting the migration of macrophages 6,7 , and the mediation of the actions of pro-inflammatory agents, such as high molecular weight kininogen to produce further pro-inflammatory agents 5,8 . C1qbp can also prevent cell damage by the elimination of C1q, and other ligands including antimicrobial peptides from the inflammatory site 9,10 .…”

Section: Introductionmentioning

confidence: 99%

Complement component 1q subcomponent binding protein in the brain of the rat

Barna

Dimén

Puska

et al. 2019

Sci Rep

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Complement component 1q subcomponent binding protein (C1qbp) is a multifunctional protein involved in immune response, energy homeostasis of cells as a plasma membrane receptor, and a nuclear, cytoplasmic or mitochondrial protein. Recent reports suggested its neuronal function, too, possibly in axon maintenance, synaptic function, and neuroplasticity. Therefore, we addressed to identify C1qbp in the rat brain using in situ hybridization histochemistry and immunolabelling at light and electron microscopic level. C1qbp has a topographical distribution in the brain established by the same pattern of C1qbp mRNA-expressing and protein-containing neurons with the highest abundance in the cerebral cortex, anterodorsal thalamic nucleus, hypothalamic paraventricular (PVN) and arcuate nuclei, spinal trigeminal nucleus. Double labelling of C1qbp with the neuronal marker NeuN, with the astrocyte marker S100, and the microglia marker Iba1 demonstrated the presence of C1qbp in neurons but not in glial cells in the normal brain, while C1qbp appeared in microglia following their activation induced by focal ischemic lesion. Only restricted neurons expressed C1qbp, for example, in the PVN, magnocellular neurons selectively contained C1qbp. Further double labelling by using the mitochondria marker Idh3a antibody suggested the mitochondrial localization of C1qbp in the brain, confirmed by correlated light and electron microscopy at 3 different brain regions. Post-embedding immunoelectron microscopy also suggested uneven C1qbp content of mitochondria in different brain areas but also heterogeneity within single neurons. These data suggest a specific function of C1qbp in the brain related to mitochondria, such as the regulation of local energy supply in neuronal cells.

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“…MCP-1 acts as a monocyte chemotactic protein, mainly secreted by monocytes, macrophages and dendritic cells (Anders et al 2018;Du et al 2016). When an inflammatory reaction occurs, it activates the chemotaxis of monocytes/macrophages, activates the expression of leukocyte adhesion molecule-1, induces the production of the cytokine IL-1, IL-6, and regulates expression of specific adhesion molecules such as CDllc and CDllb on the surface of monocyte (Anders et al 2018;Du et al 2016). Besides, as an important inflammatory initiating factor, TNF-α has the cytotoxic and multiproinflammatory effects, indicating the activation of inflammatory (Zhang et al 2011).…”

Section: Discussionmentioning

confidence: 99%

D-allose alleviates ischemia/reperfusion (I/R) injury in skin flap via MKP-1

Hou

Zhang

2020

Mol Med

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Background: D-allose was promising in the protection of ischemia/reperfusion (I/R) injury. We intended to investigate the function of D-allose in skin flap of rat followed by the injury of I/R and whether ERK signal pathway was involved in. Methods: The back flap of Wistar rats was picked up with a vascular bundle of the lateral chest wall. I/R model was made by the venous clamp for 6 h. Rats received D-allose and PD-98059, the inhibitor of ERK1/2, 30 min before modeling. Morphology of tissue was observed by HE staining. Nitric oxide (NO), myeloperoxidase (MPO), malondialdehyde (MDA) and superoxide dismutase (SOD) levels in skin flap were determined by ELISA kits. mRNA and protein levels were determined by qPCR and Western blot respectively. Results: D-allose alleviated the condition of pathological changes and raised the survival rate of skin flap injured by I/R. Moreover, D-allose suppressed NO, MPO and MDA while elevated SOD levels during I/R status. Furthermore, Dallose decreased MCP-1, TNF-α, IL-1β and IL-6 levels in skin flap injured by I/R. In addition, D-allose inhibited MKP-1 expression and activated ERK1/2 pathway in skin flap injured by I/R. PD-98059 partially counteracted D-allose effects on I/R injury. Conclusions: D-allose exerted its protective function via inhibiting MKP-1expression and further activated ERK1/2 pathway to suppress the progress of oxidative stress, inflammation and necrosis, contributing to the survival of skin flap injured by I/R. Thus, D-allose was promising in the transplantation of skin flap.

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Globular C1q receptor (p33) binds and stabilizes pro-inflammatory MCP-1: a novel mechanism for regulation of MCP-1 production and function

Cited by 11 publications

References 35 publications

CCL2: An Important Mediator Between Tumor Cells and Host Cells in Tumor Microenvironment

CCL2: An Important Mediator Between Tumor Cells and Host Cells in Tumor Microenvironment

Complement component 1q subcomponent binding protein in the brain of the rat

D-allose alleviates ischemia/reperfusion (I/R) injury in skin flap via MKP-1

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