PMID- 22773968
OWN - NLM
STAT- PubMed-not-MEDLINE
DCOM- 20120823
LR  - 20211021
IS  - 2227-4898 (Electronic)
IS  - 2222-3959 (Print)
IS  - 2222-3959 (Linking)
VI  - 5
IP  - 3
DP  - 2012
TI  - Inhibitory effect of CCR3 signal on alkali-induced corneal neovascularization.
PG  - 251-7
LID - 10.3980/j.issn.2222-3959.2012.03.01 [doi]
AB  - AIM: To investigate the effect of CC chemokine receptor 3 (CCR3) signal on 
      corneal neovascularization (CRNV) induced by alkali burn and to explore its 
      mechanism. METHODS: Specific pathogen-free male BALB/C mice (aged 6-8 weeks) were 
      randomly divided into CCR3-antagonist treated group (experimental group) and 
      control group. CRNV was induced by alkali burn in mice. The time kinetic CCR3 
      expression in injured corneas was examined by reverse transcription polymerase 
      chain reaction (RT-PCR). CCR3-antagonist (SB-328437 at different concentration of 
      125microg/mL, 250microg/mL, and 500microg/mL) was locally administrated after alkali injury. 
      The formation of CRNV was assessed by CD31 corneal whole mount staining at two 
      weeks after injury. Monocyte chemotactic protein 1 (MCP-1), monocyte chemotactic 
      protein 3 (MCP-3) expressions in the early phase after injury were quantified and 
      compared by RT-PCR. Macrophage intracorneal accumulation in the early phase after 
      injury was evaluated and compared by immunohistochemistry. RESULTS: Alkali injury 
      induced the time kinetic intracorneal CCR3 expression. 500microg/mL of 
      CCR3-antagonist treatment in the early phase but not the late phase resulted in 
      significant impaired CRNV as compared to control group (P<0.05). CCR3-antagonist 
      treatment in the early phase significantly reduced the intracorneal MCP-1 and 
      MCP-3 enhancement compare to control group at day 2 and day 4 (P<0.05). Moreover, 
      the number of intracorneal macrophage infiltration in the experimental group was 
      reduced than those in control group at day 4 (P<0.05). CONCLUSION: CCR3 signal is 
      involved in alkali-induced CRNV. CCR3-antagonist can inhibit alkali-induced CRNV 
      by reducing the intracorneal MCP-1 and MCP-3 mRNA expression and the intracorneal 
      macrophage infiltration.
FAU - Zhou, Wen-Juan
AU  - Zhou WJ
AD  - Department of Ophthalmology, the First Affiliated Hospital of Soochow University, 
      Suzhou 215006, Jiangsu Province, China.
FAU - Liu, Gao-Qin
AU  - Liu GQ
FAU - Li, Long-Biao
AU  - Li LB
FAU - Zhang, Xue-Guang
AU  - Zhang XG
FAU - Lu, Pei-Rong
AU  - Lu PR
LA  - eng
PT  - Journal Article
DEP - 20120618
PL  - China
TA  - Int J Ophthalmol
JT  - International journal of ophthalmology
JID - 101553860
PMC - PMC3388388
OTO - NOTNLM
OT  - CCR3
OT  - corneal neovascularization
OT  - macrophage
OT  - monocyte chemotactic protein 1
OT  - monocyte chemotactic protein 3
EDAT- 2012/07/10 06:00
MHDA- 2012/07/10 06:01
PMCR- 2012/06/18
CRDT- 2012/07/10 06:00
PHST- 2012/01/09 00:00 [received]
PHST- 2012/05/22 00:00 [accepted]
PHST- 2012/07/10 06:00 [entrez]
PHST- 2012/07/10 06:00 [pubmed]
PHST- 2012/07/10 06:01 [medline]
PHST- 2012/06/18 00:00 [pmc-release]
AID - ijo-05-03-251 [pii]
AID - 10.3980/j.issn.2222-3959.2012.03.01 [doi]
PST - ppublish
SO  - Int J Ophthalmol. 2012;5(3):251-7. doi: 10.3980/j.issn.2222-3959.2012.03.01. Epub 
      2012 Jun 18.