PMID- 18473828
OWN - NLM
STAT- MEDLINE
DCOM- 20090316
LR  - 20191110
IS  - 1875-5739 (Electronic)
IS  - 1567-2026 (Linking)
VI  - 5
IP  - 2
DP  - 2008 May
TI  - MIP-1alpha and MCP-1 Induce Migration of Human Umbilical Cord Blood Cells in 
      Models of Stroke.
PG  - 118-24
AB  - Monocyte chemoattractant protein-1 (MCP-1) and macrophage inflammatory protein 
      (MIP-1alpha) are implicated in monocyte infiltration into the central nervous 
      system (CNS) under pathological conditions. We previously showed that in vivo 
      human umbilical cord blood cells (HUCB) migrate toward brain injury after middle 
      cerebral artery occlusion (MCAO). We hypothesized that MCP-1 and MIP-1alpha may 
      participate in the recruitment of HUCB towards the injury. Sprague-Dawley rats 
      were subjected to middle cerebral artery occlusion (MCAO), and 24 hours later the 
      production of MCP-1 and MIP-1alpha in the brain was examined with 
      immunohistochemistry, ELISA, and western blotting. The chemotactic effect of 
      MCP-1 and MIP-1alpha, and the expression of MCP-1 receptor CCR2 and MIP-1alpha 
      receptor CCR1, CCR5 on the surface of HUCB were also examined. MCP-1 and 
      MIP-1alpha expression were significantly increased in the ischemic hemisphere of 
      brain, and significantly promoted HUCB cell migration compared to the 
      contralateral side. This cell migration was neutralized with polyclonal 
      antibodies against MCP-1 or MIP-1alpha. Also chemokine receptors were 
      constitutively expressed on the surface of HUCB cells. The data suggested that 
      the increased chemokines in the ischemic area can bind cell surface receptors on 
      HUCB, and induce cell infiltration of systemically delivered HUCB cells into the 
      CNS in vivo.
FAU - Jiang, Lixian
AU  - Jiang L
AD  - Center of Excellence for Aging & Brain Repair, MDC78, University of South 
      Florida, 12901 Bruce B. Downs Blvd, Tampa FL 33612, USA.
FAU - Newman, Mary
AU  - Newman M
FAU - Saporta, Samuel
AU  - Saporta S
FAU - Chen, Ning
AU  - Chen N
FAU - Sanberg, Cyndy
AU  - Sanberg C
FAU - Sanberg, Paul R
AU  - Sanberg PR
FAU - Willing, Alison E
AU  - Willing AE
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - United Arab Emirates
TA  - Curr Neurovasc Res
JT  - Current neurovascular research
JID - 101208439
RN  - 0 (Ccl2 protein, rat)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Chemokine CCL3)
RN  - 0 (Receptors, Chemokine)
RN  - 0 (TUBB3 protein, human)
RN  - 0 (Tubulin)
SB  - IM
MH  - Animals
MH  - Brain/cytology
MH  - Cell Movement
MH  - Cells, Cultured
MH  - Chemokine CCL2/metabolism/*therapeutic use
MH  - Chemokine CCL3/metabolism/*therapeutic use
MH  - Disease Models, Animal
MH  - Embryo, Mammalian
MH  - Fetal Blood/*cytology
MH  - Humans
MH  - Neuroglia
MH  - Neurons
MH  - Random Allocation
MH  - Rats
MH  - Rats, Sprague-Dawley
MH  - Receptors, Chemokine
MH  - Stroke/*drug therapy/*surgery
MH  - Tubulin/metabolism
EDAT- 2008/05/14 09:00
MHDA- 2009/03/17 09:00
CRDT- 2008/05/14 09:00
PHST- 2008/05/14 09:00 [pubmed]
PHST- 2009/03/17 09:00 [medline]
PHST- 2008/05/14 09:00 [entrez]
AID - 10.2174/156720208784310259 [doi]
PST - ppublish
SO  - Curr Neurovasc Res. 2008 May;5(2):118-24. doi: 10.2174/156720208784310259.