CCL2 and CXCL1 trigger calcitonin gene-related peptide release by exciting primary nociceptive neurons

Qin, Xiaomei; Wan, You; Wang, Xian

doi:10.1002/jnr.20612

Cited by 129 publications

(146 citation statements)

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“…CCL2 has been proven to cause pain in animal models or articular inflammation in several animal studies. [11][12][13][14][15] One recent study showed that CCR2/CCL2 plays a key role in balancing the bone remodelling process. 28 All these factors indicate CCL2 may act in pathogenesis or progression of OA.…”

Section: Discussionmentioning

confidence: 99%

“…12 Studies have also shown CCL2 could induce pain-related behaviours in rodents. [13][14][15] Since CCL2 is present in the osteoarthritic joint, it may serve as potential pain mediator in OA. Besides, recent studies have demonstrated that CCL2 increases vascular cell adhesion molecule 1 (VCAM-1) expression in human OA synovial fibroblasts via a cascade of signalling pathways, and CCL2-induced VCAM-1 expression promoted monocyte adhesion to human OA synovial fibroblasts.…”

Section: Introductionmentioning

confidence: 99%

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Serum and synovial fluid chemokine ligand 2/monocyte chemoattractant protein 1 concentrations correlates with symptomatic severity in patients with knee osteoarthritis

Jiang

2014

Ann Clin Biochem

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Objective: Serum and synovial fluid (SF) chemokine ligand 2 (CCL2)/monocyte chemoattractant protein 1 (MCP-1) concentrations have been identified to be increased in osteoarthritis (OA) patients. The scope of this study was to examine CCL2 concentrations in serum and SF of knee OA patients and to explore their association with patientreported symptomatic severity. Method: One hundred and sixty-one knee OA patients and 138 healthy controls were enrolled into the study from our hospital. We collected Western Ontario and McMaster Universities Arthritis Index (WOMAC) scores from OA patients and measured CCL2 concentrations in serum and SF using enzyme-linked immunosorbent assay method, and correlation between WOMAC scores and CCL2 concentrations were analysed. Results: CCL2 concentrations in SF instead of serum were independently and positively associated with self-reported greater pain (r ¼ 0.460, P < 0.001) and physical disability (r ¼ 0.561, P < 0.001) in OA patients. Conclusion: CCL2 in SF might serve as a novel and reliable biomarker for assessing symptomatic severity of OA.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Serum and synovial fluid chemokine ligand 2/monocyte chemoattractant protein 1 concentrations correlates with symptomatic severity in patients with knee osteoarthritis

Jiang

2014

Ann Clin Biochem

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“…More specifically, inhibition of PKCε decreases capsaicin-induced release of glutamate and CGRP in isolated spinal cords (52). In addition to topical capsaicin, chemokines stimulate the release of CGRP from afferent neurons in a PKC dependent manner (53). One potential mechanism by which pre-synaptic PKC activity can augment neurotransmitter release is via PKC-dependent sensitization of voltage-dependent L-type Ca2+ channels (54).…”

Section: B the Primary Afferent-spinal Cord Synapsementioning

confidence: 99%

Protein kinase C in pain: Involvement of multiple isoforms

Velázquez

Mohammad

Sweitzer

2007

Pharmacological Research

130

125

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Pain is the primary reason that people seek medical care. At present chronic unremitting pain is the third greatest health problem after heart disease and cancer. Chronic pain is an economic burden in lost wages, lost productivity, medical expenses, legal fees and compensation. Chronic pain is defined as a pain of greater than two months duration and can be of an inflammatory or neuropathic origin that can arise following nerve injury or in the absence of any apparent injury. Chronic pain is characterized by an altered pain perception that includes allodynia (a response to a normally nonnoxious stimuli), and hyperalgesia (an exaggerated response to a normally noxious stimuli). This type of pain is often insensitive to the traditional pain drugs or surgical intervention and thus the study of the cellular and molecular mechanisms that contribute to chronic pain are of the up-most importance for the development of a new generation of analgesic agents. Protein kinase C isozymes are under investigation as potential therapeutics for the treatment of chronic pain conditions. The anatomical localization of protein kinase C isozymes in both peripheral and central nervous system sites that process pain have made them the topic of basic science research for close to two decades. This review will outline the research to date on protein kinase C involvement in pain and analgesia. In addition, this review will try to synthesize these works to begin to develop a comprehensive mechanistic understanding of how protein kinase C may function as the master regulator of peripheral and central sensitization that underlies many chronic pain conditions.

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“…Chemokine receptor induced calcium signalling is not completely understood. Several inhibitors, like omega-conotoxin GVIA (an Ntype calcium channel blocker), thapsigargin (a sarcoendoplasmic reticulum Ca 2+ -ATPase inhibitor) as well as phospholipase c and protein kinase c inhibitors seem to 4 affect CCL2 and CXCL1 induced calcium response [15], giving some indication about how chemokine receptor activation is coupled to calcium signalling. However for CCR5, no characterisation of the mechanisms for the intracellular calcium release after receptor activation has been shown so far.…”

Section: Introductionmentioning

confidence: 99%

Distinct modes of molecular regulation of CCL3 induced calcium flux in monocytic cells

Cardaba

Müeller

2009

Biochemical Pharmacology

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This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain.Page 1 of 32A c c e p t e d M a n u s c r i p t 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 44 45 46 47 48 49 50 51 52 53 54 55 56 57 58 59 60 61 62 63 by MCD addition, which shows that the cholesterol content in the membrane is only one factor in determining the amount of receptor response. We show that CCR5signalling is dependant on thapsigargin-sensitive Ca 2+ stores and on activation of ryanodine receptors as well as InsP3 receptors or store-operated channels.Cholesterol depletion with MCD changes the thapsigargin sensitivity in THP-1 cells * ManuscriptPage 2 of 32 A c c e p t e d M a n u s c r i p t 1 2 3 4 5 6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28 29 30 31 32 33 34 35 36 37 38 39 40 41 42 43 44 45 46 47 48 49 50 51 52 53 54 55 56 57 58 59 60 61 62 63 64 65 2 and also alters receptor-G-protein coupling towards pertussis toxin (PTX) independent G-proteins. Cholesterol removal by MCD in THP-1 cells has far reaching consequences for receptor activation and signalling and emphasises the need for a clearer understanding of how membrane fluidity affects receptor signalling events.

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CCL2 and CXCL1 trigger calcitonin gene-related peptide release by exciting primary nociceptive neurons

Cited by 129 publications

References 47 publications

Serum and synovial fluid chemokine ligand 2/monocyte chemoattractant protein 1 concentrations correlates with symptomatic severity in patients with knee osteoarthritis

Serum and synovial fluid chemokine ligand 2/monocyte chemoattractant protein 1 concentrations correlates with symptomatic severity in patients with knee osteoarthritis

Protein kinase C in pain: Involvement of multiple isoforms

Distinct modes of molecular regulation of CCL3 induced calcium flux in monocytic cells

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