Activation of p38 MAPK in the rostral ventromedial medulla by visceral noxious inputs transmitted via the dorsal columns may contribute to pelvic organ cross-sensitization in rats with endometriosis

Z. Chen, Chen Z, Zhenping Chen, Fang Xie, Xie F, F Xie, M Bao, Bao M, Mengmeng Bao, Xuying Li, X. Li, Li X, Y Chao, Chao Y, Yi‐Ping Chao, C Lin, Chi‐Chung Lin, Lin C, Ruijuan Guo, Guo R, R Guo, C. Zhang, Zhang C, Wu A, Anshi Wu, A Wu, Y Yue, Yun Yue, Yue Y, Yun Guan, Y Guan, Wang Y, Y Wang
Neuroscience · 2015 · vol. 291 , pp. 272–278 · doi:10.1016/j.neuroscience.2015.02.021 · PMID:25701711 · W2088047143
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Visceral noxious inputs transmitted via the dorsal columns activate p38 MAPK in the rostral ventromedial medulla, contributing to pelvic organ cross-sensitization in rats with endometriosis.

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Abstract

Whether visceral organ cross-sensitization is involved in endometriosis-associated pain remains elusive. Previous studies have shown that visceral noxious stimuli may trigger a cascade of signal transductions in the rostral ventromedial medulla (RVM) via the spinal dorsal column (DC) pathway and the RVM plays a critical role in the descending control of visceral nociception. In the current study, we hypothesized that the p38 mitogen-activated protein kinase (MAPK) activation in the RVM by noxious visceral inputs from ectopic growths via the DC was involved in the development of pelvic organ cross-sensitization in established endometriosis. A rat model of experimental endometriosis was established. To examine ectopic growths-to-colon cross-sensitization, graded colorectal distention (CRD) was performed and abdominal withdrawal reflex (AWR) scores were recorded in female rats at 8weeks after the uterine or fat (control) auto-transplantation. Western blot study was carried out to examine the phosphorylated form and the total level of p38 MAPK protein in the RVM. Our results showed that lesions of bilateral DCs immediately following uterine or fat auto-transplantation in female rats significantly attenuated the later development of ectopic growths-to-colon cross-sensitization and the increased p38 MAPK activation in the RVM, as compared to sham DC lesions. Furthermore, intra-RVM microinjection of a p38 MAPK inhibitor (SB 203580), but not vehicle, in female rats with established endometriosis significantly attenuated ectopic growths-to-colon cross-sensitization and the increased activation of p38 MAPK in the RVM. These findings suggest that the noxious inputs from ectopic growths may activate p38 MAPK in the RVM via the DC, which may contribute to the development of ectopic growths-to-colon cross-sensitization in established endometriosis.

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Condition tags

endometriosis

MeSH descriptors

Colon Endometriosis Medulla Oblongata p38 Mitogen-Activated Protein Kinases Visceral Pain Adipose Tissue Adipose Tissue Adipose Tissue Animals Animals Colon Colon Disease Models, Animal Disease Models, Animal Endometriosis Endometriosis Female Female Imidazoles Imidazoles

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Papers in the corpus that this work cites (lower rings, blue) and that cite this one (upper rings, green). Dot size scales with the paper's in-corpus citation count — bigger dot = more influential within the endo/adeno field. Click a dot to open that paper. Outer rings show 2-hop neighbours — papers reached through the immediate citers/citees. [ collapse to 1-hop ]

References (34)

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