scholarly journals Microglia are Involved in Pruritus Induced by DNFB via the CX3CR1/p38 MAPK Pathway

2015 ◽  
Vol 35 (3) ◽  
pp. 1023-1033 ◽  
Author(s):  
Ying Zhang ◽  
Jia Yan ◽  
Rong Hu ◽  
Yu Sun ◽  
Yiwen Ma ◽  
...  
Keyword(s):  
Neuropathic Pain ◽  
P38 Mapk ◽  
Mapk Pathway ◽  
Intrathecal Administration ◽  
P38 Inhibitor ◽  
P38 Mapk Pathway ◽  
Chronic Itch ◽  
Repeated Applications ◽  
Chronic Pruritus

Background/Aims: Pruritus, also known as itch, is a common, unpleasant sensation that can be difficult to treat. Frequently, chronic itch is associated with the development of neuropathic pain resulting from nerve injury or insult. Previous studies have shown the involvement of spinal microglia in the development of neuropathic pain, but their role in chronic pruritus is unclear. Methods: For this study, we constructed a model of chronic pruritus in mice using repeated applications of 2, 4-dinitrofluorobenzene (DNFB) and showed prolonged scratching behavior in treated mice that continued for at least 7 d after the final DNFB treatment. Results: Scratching was accompanied by activation of spinal microglia and both were reduced by an inhibitor of microglial activity. We also showed that microglial activation entailed increased signaling in the p38 MAPK pathway, and treatment with a p38 inhibitor reduced scratching in DNFB-treated mice. We also examined the role of fractalkine/CX3CR1 signaling in the development of DNFB-induced pruritus and showed that intrathecal administration of antiserum against either CX3CR1or FKN inhibited p38 activity and decreased scratching. Conclusion: Our results suggest that microglia are involved in pruritus induced by DNFB via FKN/CX3CR1/p38MAPK pathways similar to those participating in the development of neuropathic pain.

scholarly journals Role of the CX3CR1/p38 MAPK pathway in spinal microglia for the development of neuropathic pain following nerve injury-induced cleavage of fractalkine

2007 ◽  
Vol 21 (5) ◽  
pp. 642-651 ◽  
Author(s):  
Zhi-Ye Zhuang ◽  
Yasuhiko Kawasaki ◽  
Ping-Heng Tan ◽  
Yeong-Ray Wen ◽  
Jing Huang ◽  
...  
Keyword(s):  
Neuropathic Pain ◽  
Nerve Injury ◽  
P38 Mapk ◽  
Mapk Pathway ◽  
P38 Mapk Pathway

Role of the p38 MAPK Pathway in Induction of iNOS Expression in Human Leukocytes

2008 ◽  
Vol 56 (1) ◽  
pp. 83-89 ◽  
Author(s):  
Ewa Jablonska ◽  
Wioletta Ratajczak ◽  
Jakub Jablonski
Keyword(s):  
P38 Mapk ◽  
Mapk Pathway ◽  
Inos Expression ◽  
Human Leukocytes ◽  
P38 Mapk Pathway

Anti-inflammatory role of Leptin in glial cells through p38 MAPK pathway inhibition

2017 ◽  
Vol 69 (3) ◽  
pp. 409-418 ◽  
Author(s):  
Iván Patraca ◽  
Nohora Martínez ◽  
Oriol Busquets ◽  
Aleix Martí ◽  
Ignacio Pedrós ◽  
...  
Keyword(s):  
P38 Mapk ◽  
Glial Cells ◽  
Mapk Pathway ◽  
P38 Mapk Pathway ◽  
Anti Inflammatory ◽  
Pathway Inhibition

scholarly journals Estrogen Enhances Matrix Synthesis in Nucleus Pulposus Cell through the Estrogen Receptor β-p38 MAPK Pathway

2016 ◽  
Vol 39 (6) ◽  
pp. 2216-2226 ◽  
Author(s):  
Pei Li ◽  
Yuan Xu ◽  
Yibo Gan ◽  
Liyuan Wang ◽  
Bin Ouyang ◽  
...  
Keyword(s):  
Estrogen Receptor ◽  
Signaling Pathway ◽  
P38 Mapk ◽  
Mapk Pathway ◽  
Mapk Signaling ◽  
Mapk Signaling Pathway ◽  
Matrix Synthesis ◽  
P38 Mapk Pathway ◽  
Collagen Ii

Background/Aims: Matrix homeostasis within the disc nucleus pulposus (NP) tissue is important for disc function. Increasing evidence indicates that sex hormone can influence the severity of disc degeneration. This study was aimed to study the role of 17β-estradiol (E2) in NP matrix synthesis and its underlying mechanism. Methods: Rat NP cells were cultured with (10-5, 10-7 and 10-9 M) or without (control) E2 for48 hours. The estrogen receptor (ER)-β antagonist PHTPP and ERβ agonist ERB 041 were used to investigate the role mediated by ERβ. The p38 MAPK inhibitor SB203580 was used to investigate the role of p38 MAPK signaling pathway. Gene and protein expression of SOX9, aggrecan and collagen II, glycosaminoglycan (GAG) content, and immunostaining assay for aggrecan and collagen II were analyzed to evaluate matrix production in rat NP cells. Results: E2 enhanced NP matrix synthesis in a concentration-dependent manner regarding gene and proetin expression of SOX9, aggrecan and collagen II, protein deposition of aggrecan and collagen II, and GAG content. Moreover, activation of p38 MAPK signaling pathway was increased with elevating E2 concentration. Further analysis indicated that ERB 041 and PHTPP could respectively enhance and suppress effects of E2 on matrix synthesis in NP cells, as well as activation of p38 MAPK pathway. Additionally, inhibition of p38 MAPK signaling pathway significantly abolished the effects of E2 on matrix synthesis. Conclusion: E2 can enhance matrix synthesis of NP cells and the ERβ/p38 MAPK pathway is involved in this regulatory process.

The role of Rho-GEF Trio in regulating tooth root development through the p38 MAPK pathway

2018 ◽  
Vol 372 (2) ◽  
pp. 158-167 ◽  
Author(s):  
Huimin Chen ◽  
Shuyu Guo ◽  
Yang Xia ◽  
Lichan Yuan ◽  
Mengting Lu ◽  
...  
Keyword(s):  
P38 Mapk ◽  
Root Development ◽  
Mapk Pathway ◽  
Tooth Root ◽  
P38 Mapk Pathway ◽  
Rho Gef

The role of p38 MAPK pathway in p53 compromised state and telomere mediated DNA damage response

2018 ◽  
Vol 836 ◽  
pp. 89-97 ◽  
Author(s):  
Shomereeta Roy ◽  
Souvick Roy ◽  
Aarti Rana ◽  
Yusuf Akhter ◽  
Manoor Prakash Hande ◽  
...  
Keyword(s):  
Dna Damage ◽  
P38 Mapk ◽  
Dna Damage Response ◽  
Mapk Pathway ◽  
P38 Mapk Pathway ◽  
Damage Response

scholarly journals The role of the MKK6/p38 MAPK pathway in Wip1-dependent regulation of ErbB2-driven mammary gland tumorigenesis

Oncogene ◽  
2006 ◽  
Vol 26 (17) ◽  
pp. 2502-2506 ◽  
Author(s):  
O N Demidov ◽  
C Kek ◽  
S Shreeram ◽  
O Timofeev ◽  
A J Fornace ◽  
...  
Keyword(s):  
Mammary Gland ◽  
P38 Mapk ◽  
Mapk Pathway ◽  
P38 Mapk Pathway

scholarly journals Role of p38–MAPK pathway in the effects of high-magnitude compression on nucleus pulposus cell senescence in a disc perfusion culture

2017 ◽  
Vol 37 (5) ◽  
Author(s):  
Lianglong Pang ◽  
Pei Li ◽  
Ruijie Zhang ◽  
Yuan Xu ◽  
Lei Song ◽  
...  
Keyword(s):  
Nucleus Pulposus ◽  
P38 Mapk ◽  
Ex Vivo ◽  
Mapk Pathway ◽  
Cell Senescence ◽  
Bioreactor Culture ◽  
Pathological Feature ◽  
High Magnitude ◽  
P38 Mapk Pathway

Nucleus pulposus (NP) cell senescence is a typical pathological feature within the degenerative intervertebral disc. As a potential inducing and aggregating factor of disc degeneration, mechanical overloading affects disc biology in multiple ways. The present study was to investigate the NP cell senescence-associated phenotype under intermittent high compression in an ex vivo disc bioreactor culture, and the role of the p38–MAPK pathway in this regulatory process. Porcine discs were cultured in culture chambers of a self-developed mechanically active bioreactor and subjected to different magnitudes of dynamic compression (low-magnitude and high-magnitude: 0.1 and 1.3 MPa at a frequency of 1.0 Hz for 2 h per day respectively) for 7 days. Non-compressed discs were used as controls. The inhibitor SB203580 was used to study the role of the p38–MAPK pathway in this process. Results showed that intermittent high-magnitude compression clearly induced senescence-associated changes in NP cells, such as increasing β-galactosidase-positive NP cells, decreasing PCNA-positive NP cells, promoting the formation of senescence-associated heterochromatic foci (SAHF), up-regulating the expression of senescence markers (p16 and p53), and attenuating matrix production. However, inhibition of the p38–MAPK pathway partly attenuated the effects of intermittent high-magnitude (1.3 MPa) compression on those described NP cell senescence-associated parameters. In conclusion, intermittent high-magnitude compression can induce NP cell senescence-associated changes in an ex vivo disc bioreactor culture, and the p38–MAPK pathway is involved in this process.

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