PMID- 16174730
OWN - NLM
STAT- MEDLINE
DCOM- 20051121
LR  - 20220310
IS  - 0027-8424 (Print)
IS  - 1091-6490 (Electronic)
IS  - 0027-8424 (Linking)
VI  - 102
IP  - 39
DP  - 2005 Sep 27
TI  - Excitatory monocyte chemoattractant protein-1 signaling is up-regulated in 
      sensory neurons after chronic compression of the dorsal root ganglion.
PG  - 14092-7
AB  - Neuronal hyperexcitability in both injured and adjacent uninjured neurons is 
      associated with states of chronic injury and pain and is likely subject to 
      neuroinflammatory processes. Chronic inflammatory responses are largely 
      orchestrated by chemokines. One chemokine, monocyte chemoattractant protein-1 
      (MCP-1), in the presence of its cognate receptor, the beta chemokine receptor 2 
      (CCR2), produces neural activity in dissociated neuronal cultures of neonatal 
      dorsal root ganglion (DRG) neurons. Using a neuropathic pain model, chronic 
      compression of the DRG (CCD), we compared anatomically separate populations of 
      noncompressed lumbar DRG (L3/L6) with compressed lumbar DRG (L4/L5) for changes 
      in the gene expression of CCR2. In situ hybridization revealed that CCR2 mRNA was 
      up-regulated in neurons and nonneuronal cells present in both compressed L4/L5 
      and ipsilateral noncompressed L3/L6 DRGs at postoperative day 5 (POD5). The total 
      percentages of compressed and noncompressed neurons exhibiting CCR2 mRNA 
      transcripts in L3, L5, and L6 DRG were 33 +/- 3.5%, 49 +/- 6.2%, and 41 +/- 5.6%, 
      respectively, and included cell bodies of small, medium, and large size. In 
      addition, the preferred CCR2 ligand, MCP-1, was up-regulated by POD5 in both 
      compressed L4/L5 and noncompressed L3/L6 DRG neurons. Application of MCP-1 to the 
      cell bodies of the intact formerly compressed DRG in vitro produced potent 
      excitatory effects not observed in control ganglia. MCP-1/CCR2 signaling is 
      directly involved with a chronic compression injury and may contribute to 
      associated neuronal hyperexcitability and neuropathic pain.
FAU - White, Fletcher A
AU  - White FA
AD  - Department of Cell Biology, Neurobiology, and Anatomy, and Anesthesiology, 
      Stritch School of Medicine, Loyola University Chicago, Maywood, IL 60153, USA. 
      fwhite@lumc.edu
FAU - Sun, Jihu
AU  - Sun J
FAU - Waters, Stephen M
AU  - Waters SM
FAU - Ma, Chao
AU  - Ma C
FAU - Ren, Dongjun
AU  - Ren D
FAU - Ripsch, Matthew
AU  - Ripsch M
FAU - Steflik, Jeremy
AU  - Steflik J
FAU - Cortright, Daniel N
AU  - Cortright DN
FAU - Lamotte, Robert H
AU  - Lamotte RH
FAU - Miller, Richard J
AU  - Miller RJ
LA  - eng
GR  - MH040165/MH/NIMH NIH HHS/United States
GR  - NS014624/NS/NINDS NIH HHS/United States
GR  - R01 NS049136/NS/NINDS NIH HHS/United States
GR  - R01 DA013141/DA/NIDA NIH HHS/United States
GR  - NS038317/NS/NINDS NIH HHS/United States
GR  - DA01341/DA/NIDA NIH HHS/United States
GR  - R37 MH040165/MH/NIMH NIH HHS/United States
GR  - R01 NS014624/NS/NINDS NIH HHS/United States
GR  - R01 NS043095/NS/NINDS NIH HHS/United States
GR  - NS043095/NS/NINDS NIH HHS/United States
PT  - Journal Article
PT  - Research Support, N.I.H., Extramural
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
DEP - 20050920
PL  - United States
TA  - Proc Natl Acad Sci U S A
JT  - Proceedings of the National Academy of Sciences of the United States of America
JID - 7505876
RN  - 0 (Ccr2 protein, rat)
RN  - 0 (Chemokine CCL2)
RN  - 0 (RNA, Messenger)
RN  - 0 (Receptors, CCR2)
RN  - 0 (Receptors, Chemokine)
SB  - IM
MH  - Animals
MH  - Chemokine CCL2/analysis/*metabolism
MH  - Female
MH  - Ganglia, Spinal/metabolism/*pathology
MH  - Gene Expression
MH  - Lumbosacral Region/pathology
MH  - Macrophages/metabolism
MH  - Neurons, Afferent/chemistry/*metabolism/pathology
MH  - RNA, Messenger/analysis/metabolism
MH  - Radiculopathy/*metabolism/pathology
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Receptors, CCR2
MH  - Receptors, Chemokine/genetics/*metabolism
MH  - *Up-Regulation
PMC - PMC1236537
EDAT- 2005/09/22 09:00
MHDA- 2005/12/13 09:00
PMCR- 2006/03/27
CRDT- 2005/09/22 09:00
PHST- 2005/09/22 09:00 [pubmed]
PHST- 2005/12/13 09:00 [medline]
PHST- 2005/09/22 09:00 [entrez]
PHST- 2006/03/27 00:00 [pmc-release]
AID - 0503496102 [pii]
AID - 010214092 [pii]
AID - 10.1073/pnas.0503496102 [doi]
PST - ppublish
SO  - Proc Natl Acad Sci U S A. 2005 Sep 27;102(39):14092-7. doi: 
      10.1073/pnas.0503496102. Epub 2005 Sep 20.