PMID- 12444600
OWN - NLM
STAT- MEDLINE
DCOM- 20030124
LR  - 20071115
IS  - 0360-4012 (Print)
IS  - 0360-4012 (Linking)
VI  - 70
IP  - 6
DP  - 2002 Dec 15
TI  - Chemokine regulation of macrophage recruitment into the olfactory epithelium 
      following target ablation: involvement of macrophage inflammatory protein-1alpha 
      and monocyte chemoattractant protein-1.
PG  - 784-93
AB  - Target ablation by olfactory bulbectomy synchronizes the degenerative cell death 
      of olfactory receptor neurons (ORNs), infiltration of macrophages, and 
      proliferation of progenitor cells, leading to neurogenesis, ORN replacement, and 
      regeneration of the sensory epithelium. Although macrophages participate in the 
      degenerative and regenerative events, little is known of the molecular and 
      cellular mechanisms associated with their recruitment during the earliest period 
      following target ablation. Macrophage inflammatory protein-1alpha (MIP-1alpha) 
      and monocyte chemoattractant protein-1 (MCP-1), which are members of the CC or 
      beta-chemokine subfamily, are chemoattractants for monocytes/macrophages. Shortly 
      after target ablation, the protein and mRNA levels for MIP-1alpha and MCP-1 were 
      up-regulated, showing peak expression levels from 16 hr to 3 days post-OBX; this 
      coincided with the pattern of infiltration of activated F4/80(+) macrophages. The 
      mRNAs for MIP-1alpha and MCP-1, as well as their cognate receptors CCR1 and CCR2, 
      respectively, were localized in resident and infiltrating macrophages in numbers 
      commensurate with those of F4/80-immunopositive macrophages in adjacent tissue 
      sections. The mRNA(+) macrophages were localized within olfactory epithelial 
      compartments that corresponded with their proposed functions associated with 
      phagocytosis, proliferation, and infiltration. Our data support the hypothesis 
      that MIP-1alpha and MCP-1 are chemoattractant chemokines associated with the 
      recruitment of macrophages into the olfactory epithelium shortly after target 
      ablation.
CI  - Copyright 2002 Wiley-Liss, Inc.
FAU - Getchell, Thomas V
AU  - Getchell TV
AD  - Sanders-Brown Center on Aging, University of Kentucky College of Medicine, 
      Lexington, Kentucky 40536-0230, USA. tgetche@pop.uky.edu
FAU - Subhedar, Nishikant K
AU  - Subhedar NK
FAU - Shah, Dharmen S
AU  - Shah DS
FAU - Hackley, Grant
AU  - Hackley G
FAU - Partin, James V
AU  - Partin JV
FAU - Sen, Goutam
AU  - Sen G
FAU - Getchell, Marilyn L
AU  - Getchell ML
LA  - eng
GR  - R01 AG-16823/AG/NIA NIH HHS/United States
PT  - Journal Article
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - J Neurosci Res
JT  - Journal of neuroscience research
JID - 7600111
RN  - 0 (Chemokine CCL2)
RN  - 0 (Chemokine CCL3)
RN  - 0 (Chemokine CCL4)
RN  - 0 (Chemotactic Factors)
RN  - 0 (Macrophage Inflammatory Proteins)
RN  - 0 (RNA, Messenger)
RN  - 0 (Receptors, Chemokine)
SB  - IM
MH  - Animals
MH  - Axotomy
MH  - Cell Movement/physiology
MH  - Chemokine CCL2/*biosynthesis/genetics
MH  - Chemokine CCL3
MH  - Chemokine CCL4
MH  - Chemotactic Factors
MH  - Enzyme-Linked Immunosorbent Assay
MH  - Fluorescent Antibody Technique
MH  - In Situ Hybridization
MH  - Macrophage Inflammatory Proteins/*biosynthesis/genetics
MH  - Macrophages/*cytology/metabolism
MH  - Mice
MH  - Mice, Inbred C57BL
MH  - Olfactory Bulb/physiology
MH  - Olfactory Mucosa/*cytology/innervation/metabolism
MH  - Polymerase Chain Reaction
MH  - RNA, Messenger/*analysis
MH  - Receptors, Chemokine/genetics/metabolism
MH  - Time Factors
MH  - Up-Regulation
EDAT- 2002/11/22 04:00
MHDA- 2003/01/25 04:00
CRDT- 2002/11/22 04:00
PHST- 2002/11/22 04:00 [pubmed]
PHST- 2003/01/25 04:00 [medline]
PHST- 2002/11/22 04:00 [entrez]
AID - 10.1002/jnr.10432 [doi]
PST - ppublish
SO  - J Neurosci Res. 2002 Dec 15;70(6):784-93. doi: 10.1002/jnr.10432.