The P2X7 Receptor, Cathepsin S and Fractalkine in the Trigeminal Subnucleus Caudalis Signal Persistent Hypernociception in Temporomandibular Rat Joints

Bonfante, Ricardo; Napimoga, Marcelo Henrique; Macedo, Cristina Gomes de; Abdalla, Henrique Ballassini; Pieroni, Victor Luís; Clemente-Napimoga, Juliana Trindade

doi:10.1016/j.neuroscience.2018.09.005

Cited by 25 publications

(22 citation statements)

References 43 publications

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“…The results indicate that in this model the FKN/CX3CR1 axis does not act as a pronociceptive factor at the trigeminal level in STZ rats (36). The contrasting findings from this model (showing increases in FKN/CX3CR1 with reduced nociceptive behaviour) compared to others (showing increases in expression of FKN/CX3CR1 linked with increased nociceptive responses) (34,35) illustrates the complexity of nociceptive mechanisms in different pain conditions and indicates variability between different pain models. Interestingly, contrasting evidence from studies in the spinal system of STZ mice indicates that FKN/CX3CR1 could participate as a pronociceptive factor, as shown by paw withdrawal thresholds measured in KO and WT CX3CR1 STZ mice (77).…”

Section: Other Evidence Of Chemokine Activation In Animal Models Of Painmentioning

confidence: 69%

“…Bonfante et al ( 34 ) investigated the acute (24 h) and persistent (7 and 14 days) hypernociceptive response to albumin-induced arthritis in the TMJ assessed by a formalin test in rats. Protein levels extracted from the Vc of animals in the persistent group showed significantly higher expression of P2X7, cathepsin S (CatS), and FKN, compared with the control group and the acute hypernociception group.…”

Section: Other Evidence Of Chemokine Activation In Animal Models Of Painmentioning

confidence: 99%

“…The results suggest that the increased expression of FKN in the central nervous system (Vc) could be implicated in the maintenance of nociception. Interestingly, overexpression was not linked to microglial activation in Vc, as observed by the lack of significant change in protein expression of CD11b and p38MAPK ( 34 ). Whereas, in the spinal system, activation of the CatS/FKN pathway has been shown to be related to higher levels of CD11b and p38MAPK ( 75 , 76 ), further studies are needed to investigate the cellular localisation of the components of the CatS/FKN/CX3CR1 pathway in Vc and to establish the participation of microglia in this pathway in Vc.…”

Section: Other Evidence Of Chemokine Activation In Animal Models Of Painmentioning

confidence: 99%

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Chemokines and Pain in the Trigeminal System

2021

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Chemotactic cytokines or chemokines are a large family of secreted proteins able to induce chemotaxis. Chemokines are categorized according to their primary amino acid sequence, and in particular their cysteine residues that form disulphide bonds to maintain the structure: CC, CXC, CX3C, and XC, in which X represents variable amino acids. Among their many roles, chemokines are known to be key players in pain modulation in the peripheral and central nervous systems. Thus, they are promising candidates for novel therapeutics that could replace current, often ineffective treatments. The spinal and trigeminal systems are intrinsically different beyond their anatomical location, and it has been suggested that there are also differences in their sensory mechanisms. Hence, understanding the different mechanisms involved in pain modulation for each system could aid in developing appropriate pharmacological alternatives. Here, we aim to describe the current landscape of chemokines that have been studied specifically with regard to trigeminal pain. Searching PubMed and Google Scholar, we identified 30 reports describing chemokines in animal models of trigeminal pain, and 15 reports describing chemokines involved in human pain associated with the trigeminal system. This review highlights the chemokines studied to date at different levels of the trigeminal system, their cellular localization and, where available, their role in a variety of animal pain models.

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Section: Other Evidence Of Chemokine Activation In Animal Models Of Painmentioning

confidence: 69%

Section: Other Evidence Of Chemokine Activation In Animal Models Of Painmentioning

confidence: 99%

Section: Other Evidence Of Chemokine Activation In Animal Models Of Painmentioning

confidence: 99%

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Chemokines and Pain in the Trigeminal System

2021

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“…As a papain with the richest functions in the mammalian elastase system, cathepsin S is of great value in numerous pathophysiological processes, such as gene transcription and regulation through controlling the promoter of protein genes (9). Therefore, it is considered as the most common candidate gene for the occurrence and development of atherosclerosis (10).…”

Section: Discussionmentioning

confidence: 99%

Correlation of cathepsin S with coronary stenosis degree, carotid thickness, blood pressure, glucose and lipid metabolism and vascular endothelial function in atherosclerosis

Huang

Cao

2019

Exp Ther Med

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Correlation of cathepsin S with coronary stenosis degree, carotid thickness, blood pressure, glucose and lipid metabolism, and vascular endothelial function in patients with atherosclerosis was investigated. Data from 120 patients with increased cathepsin S levels (increased group) and 120 subjects with normal cathepsin S levels (normal group) were retrospectively analyzed. The serum cathepsin S level and Gensini score were compared between the healthy subjects and patients with coronary atherosclerotic heart disease, and the correlation between serum cathepsin S level and Gensini score was analyzed. The carotid thickness, mean arterial pressure, and indexes related to glucose and lipid metabolism, as well as vascular endothelial function were compared between the two groups. The correlation of the serum cathepsin S level with carotid intima-media thickness (IMT), mean arterial pressure, fasting blood glucose, total cholesterol (TC) and nitric oxide (NO) was also investigated. Patients with multi-vessel coronary artery disease (CAD) had higher serum cathepsin S level than those with double-vessel and single-vessel disease, and higher level than that of healthy subjects. The Gensini score of patients with multi-vessel CAD was higher than that of patients with double-vessel and single-vessel disease, as well as that of healthy subjects. The serum cathepsin S level was positively correlated with the Gensini score. Patients with increased cathepsin S level had greater IMT, higher mean arterial pressure, fasting blood glucose, fasting insulin (FINS), triglyceride (TG), TC, and endothelin-1 (ET-1), however, lower NO level than those of healthy subjects. The serum cathepsin S level was positively correlated with IMT, mean arterial pressure, fasting blood glucose, and TC, however, it was negatively correlated with the NO level. In conclusion, as the serum cathepsin S level is elevated, the coronary stenosis is aggravated, the carotid thickness and blood pressure are increased, and the glucose and lipid metabolism, as well as vascular endothelial function are significantly abnormal.

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“…In 2018, Bonfante et al reported an increased protein level of P2X 7 in the trigeminal subnucleus caudalis in a persistent model of inflammatory hypernociception induced by arthritis in the TMJ of rats. Expression of P2X 7 was found in CX3CR1+/CCR2− microglial cells 95. As a key player in IL-1 processing and release, P2X 7 up-regulates the secretion of IL-1β from monocytes, which induces the transcription of cyclooxygenase-2 (COX-2) and iNOS in CNS and contributes to generation and maintenance of pain [96][97][98].…”

mentioning

confidence: 99%

Neuroimmune interactions in painful TMD: Mechanisms and treatment implications

Zhou

Xiong

et al. 2021

Journal of Leukocyte Biology

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The underlying mechanisms and treatment of painful temporomandibular disorders (TMDs) are important but understudied topics in craniofacial research. As a group of musculoskeletal diseases, the onset of painful TMD is proved to be a result of disturbance of multiple systems. Recently, emerging evidence has revealed the involvement of neuroimmune interactions in painful TMD. Inflammatory factors play an important role in peripheral sensitization of temporomandibular joint (TMJ), and neurogenic inflammation in turn enhances TMJs dysfunction in TMD. Furthermore, centralized neuroimmune communications contribute to neuron excitability amplification, leading to pain sensitization, and is also responsible for chronic TMD pain and other CNS symptoms. Therapeutics targeting neuroimmune interactions may shed light on new approaches for treating TMD. In this review, we will discuss the role of neuroimmune interactions in the onset of painful TMD from the peripheral and centralized perspectives, and how understanding this mechanism could provide new treatment options. Insights into the neuroimmune interactions within TMJs and painful TMD would broaden the knowledge of mechanisms and treatments of this multifactorial disease.

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The P2X7 Receptor, Cathepsin S and Fractalkine in the Trigeminal Subnucleus Caudalis Signal Persistent Hypernociception in Temporomandibular Rat Joints

Cited by 25 publications

References 43 publications

Chemokines and Pain in the Trigeminal System

Chemokines and Pain in the Trigeminal System

Correlation of cathepsin S with coronary stenosis degree, carotid thickness, blood pressure, glucose and lipid metabolism and vascular endothelial function in atherosclerosis

Neuroimmune interactions in painful TMD: Mechanisms and treatment implications

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