RGD Reference Report - Calpain-2 contributes to neuropathic pain following motor nerve injury via up-regulating interleukin-6 in DRG neurons. - Rat Genome Database

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Calpain-2 contributes to neuropathic pain following motor nerve injury via up-regulating interleukin-6 in DRG neurons.

Authors: Zang, Ying  Chen, Shao-Xia  Liao, Guang-Jie  Zhu, He-Quan  Wei, Xu-Hong  Cui, Yu  Na, Xiao-Dong  Pang, Rui-Ping  Xin, Wen-Jun  Zhou, Li-Jun  Liu, Xian-Guo 
Citation: Zang Y, etal., Brain Behav Immun. 2015 Feb;44:37-47. doi: 10.1016/j.bbi.2014.08.003. Epub 2014 Aug 20.
RGD ID: 13792585
Pubmed: PMID:25150005   (View Abstract at PubMed)
DOI: DOI:10.1016/j.bbi.2014.08.003   (Journal Full-text)

Motor nerve injury by L5 ventral root transection (L5-VRT) initiates interleukin-6 (IL-6) up-regulation in primary afferent system contributing to neuropathic pain. However, the early upstream regulatory mechanisms of IL-6 after L5-VRT are still unknown. Here, we monitored both the activity of calpain, a calcium-dependent protease suggested as one of the earliest mediators for cytokine regulation, and the expression of IL-6 in bilateral L4-L6 dorsal root ganglias (DRGs) soon after L5-VRT. We found that the protein level of calpain-2 in DRGs, but not calpain-1 was increased transiently in the first 10 min(-1)h ipsilaterally and 20 min(-1)h contralaterally after L5-VRT, long before mechanical allodynia was initiated (5-15 h ipsilaterally and 15 h(-1)d contralaterally). The early activation of calpain evaluated by the generation of spectrin breakdown products (SBDP) correlated well with IL-6 up-regulation in bilateral DRGs. Double immunofluorescence staining revealed that almost all the calpain-2 positive neurons expressed IL-6, indicating an association between calpain-2 and IL-6. Inhibition of calpain by pre-treatment with MDL28170 (25mg/kg, i.p.) attenuated the rat mechanical allodynia and prevented the early up-regulation of IL-6 following L5-VRT. Addition of exogenous calpain-2 onto the surface of left L5 DRG triggered a temporal allodynia and increased IL-6 in bilateral DRGs simultaneously. Taken together, the early increase of calpain-2 in L5-VRT rats might be responsible for the induction of allodynia via up-regulating IL-6 in DRG neurons.



RGD Manual Disease Annotations    Click to see Annotation Detail View

  
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
CAPN2HumanHyperalgesia treatmentISOCapn2 (Rattus norvegicus)associated with Peripheral Nerve InjuriesRGD 
Capn2RatHyperalgesia treatmentIMP associated with Peripheral Nerve InjuriesRGD 
Capn2MouseHyperalgesia treatmentISOCapn2 (Rattus norvegicus)associated with Peripheral Nerve InjuriesRGD 
CAPN2HumanPeripheral Nerve Injuries  ISOCapn2 (Rattus norvegicus) RGD 
Capn2RatPeripheral Nerve Injuries  IEP  RGD 
Capn2MousePeripheral Nerve Injuries  ISOCapn2 (Rattus norvegicus) RGD 

Gene Ontology Annotations    Click to see Annotation Detail View

Biological Process

  
Object SymbolSpeciesTermQualifierEvidenceWithNotesSourceOriginal Reference(s)
Capn2Ratbehavioral response to pain  IDA  RGD 
Capn2Ratregulation of interleukin-6 production  IMP  RGD 

Objects Annotated

Genes (Rattus norvegicus)
Capn2  (calpain 2)

Genes (Mus musculus)
Capn2  (calpain 2)

Genes (Homo sapiens)
CAPN2  (calpain 2)


Additional Information