PMID- 22956618
OWN - NLM
STAT- MEDLINE
DCOM- 20121213
LR  - 20130109
IS  - 1552-5783 (Electronic)
IS  - 0146-0404 (Linking)
VI  - 53
IP  - 10
DP  - 2012 Sep 28
TI  - The effect of monocyte chemoattractant protein-1/CC chemokine ligand 2 on aqueous 
      humor outflow facility.
PG  - 6702-7
AB  - PURPOSE: To investigate the effect of monocyte chemoattractant protein-1 
      (MCP-1)/CC chemokine ligand 2 on aqueous humor outflow facility. METHODS: Aqueous 
      humor outflow facility was measured in enucleated porcine eyes in a constant 
      pressure perfusion system with or without MCP-1 (1600 ng/mL). Expression of CCR2, 
      an MCP-1 receptor, in Schlemm's canal endothelial (SCE) cells was examined by 
      reverse transcription-polymerase chain reaction (RT-PCR) assay. The effect of 
      MCP-1 (0-1600 ng/mL) on SCE cell viability was evaluated using a WST-8 assay. The 
      effect of MCP-1 (0-800 ng/mL) on SCE-cell monolayer permeability was evaluated 
      with or without a CCR2 antagonist (10 nM) by measuring transendothelial 
      electrical resistance (TEER). The intracellular localization of the gap junction 
      protein ZO-1 was analyzed by immunofluorescence staining of SCE cells. RESULTS: 
      The aqueous humor outflow facility increased significantly from basal levels at 
      80 minutes after perfusion with MCP-1 compared with control eyes (21.2% +/- 6.6% 
      [MCP-1] vs. 5.7 +/- 2.5% [control]; P = 0.048). CCR2 was detected by RT-PCR. Cell 
      viability was not affected by MCP-1 treatment. TEER of SCE-cell monolayer at 3 
      hours after treatment with 800 ng/mL MCP-1 decreased by 21.6 +/- 1.7% compared with 
      controls (P = 0.014), and the TEER-decreasing effects of MCP-1 were attenuated by 
      a CCR2 antagonist. Immunocytochemical staining revealed a modest disruption of 
      ZO-1 in MCP-1-treated SCE cells. CONCLUSIONS: The present results revealed that 
      MCP-1 increased aqueous humor outflow facility and decreased TEER via CCR2. These 
      findings suggest that MCP-1 modulates aqueous humor outflow through the 
      conventional pathway.
FAU - Tsuboi, Naoko
AU  - Tsuboi N
AD  - Department of Ophthalmology, Faculty of Life Sciences, Kumamoto University, 1-1-1 
      Honjo, Kumamoto, Japan.
FAU - Inoue, Toshihiro
AU  - Inoue T
FAU - Kawai, Motofumi
AU  - Kawai M
FAU - Inoue-Mochita, Miyuki
AU  - Inoue-Mochita M
FAU - Fujimoto, Tomokazu
AU  - Fujimoto T
FAU - Awai-Kasaoka, Nanako
AU  - Awai-Kasaoka N
FAU - Yoshida, Akitoshi
AU  - Yoshida A
FAU - Tanihara, Hidenobu
AU  - Tanihara H
LA  - eng
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20120928
PL  - United States
TA  - Invest Ophthalmol Vis Sci
JT  - Investigative ophthalmology & visual science
JID - 7703701
RN  - 0 (Chemokine CCL2)
SB  - IM
MH  - Animals
MH  - Aqueous Humor/*drug effects/metabolism
MH  - Cells, Cultured
MH  - Chemokine CCL2/*pharmacology
MH  - Immunohistochemistry
MH  - Swine
MH  - Trabecular Meshwork/cytology/drug effects/*physiology
EDAT- 2012/09/08 06:00
MHDA- 2012/12/14 06:00
CRDT- 2012/09/08 06:00
PHST- 2012/09/08 06:00 [entrez]
PHST- 2012/09/08 06:00 [pubmed]
PHST- 2012/12/14 06:00 [medline]
AID - iovs.12-10376 [pii]
AID - 10.1167/iovs.12-10376 [doi]
PST - epublish
SO  - Invest Ophthalmol Vis Sci. 2012 Sep 28;53(10):6702-7. doi: 10.1167/iovs.12-10376.