PMID- 11549610
OWN - NLM
STAT- MEDLINE
DCOM- 20011011
LR  - 20181113
IS  - 0002-9440 (Print)
IS  - 1525-2191 (Electronic)
IS  - 0002-9440 (Linking)
VI  - 159
IP  - 3
DP  - 2001 Sep
TI  - Thrombin regulates chemokine induction during human retinal pigment epithelial 
      cell/monocyte interaction.
PG  - 1171-80
AB  - Thrombin, an important clotting factor, extravasates at sites of blood-retina 
      barrier breakdown that is often associated with many retinal diseases. Here we 
      investigated the effects of thrombin on human retinal pigment epithelial (HRPE) 
      cells, monocytes, and HRPE cell/monocyte co-cultures. Thrombin induced secretion 
      and mRNA expression of HRPE interleukin (IL)-8 and monocyte chemoattractant 
      protein-1 (MCP-1). Thrombin also enhanced IL-8 and MCP-1 by HRPE cell/monocyte 
      co-cultures, by apparently enhancing cell-cell contact mechanisms. The thrombin 
      effects on IL-6 secretion were similar to those on chemokine secretion. 
      Thrombin-induced chemokines by co-cultures were inhibited by anti-tumor necrosis 
      factor-alpha (TNF-alpha) antibody, but not by anti-IL-1beta antibody. TNF-alpha 
      was detected in cell lysates of monocytes detached from HRPE cells after 
      co-culture stimulation with thrombin. HRPE cells mainly produced these 
      chemokines. However, thrombin generally potentiated exogenous IL-1beta- and 
      TNF-alpha-induced chemokine production by HRPE cells, monocytes, and co-cultures. 
      Interferon-gamma potentiated chemokine secretion by co-cultures with or without 
      thrombin. Our results indicate that thrombin may cause leukocyte recruitment by 
      inducing HRPE cell and monocyte chemokine and by enhancing HRPE cell/monocyte 
      interactions, in part because of monocyte TNF-alpha induction, suggesting 
      important mechanisms for ocular inflammation during blood-retina barrier 
      breakdown and intra-ocular hemorrhage.
FAU - Yoshida, A
AU  - Yoshida A
AD  - Department of Ophthalmology, University of Michigan, Ann Arbor, Michigan 48105, 
      USA.
FAU - Elner, S G
AU  - Elner SG
FAU - Bian, Z M
AU  - Bian ZM
FAU - Kunkel, S L
AU  - Kunkel SL
FAU - Lukacs, N W
AU  - Lukacs NW
FAU - Elner, V M
AU  - Elner VM
LA  - eng
GR  - EY007003/EY/NEI NIH HHS/United States
GR  - EY09441/EY/NEI NIH HHS/United States
GR  - R01 EY009441/EY/NEI NIH HHS/United States
GR  - P30 EY007003/EY/NEI NIH HHS/United States
GR  - F31 EY007003/EY/NEI NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Am J Pathol
JT  - The American journal of pathology
JID - 0370502
RN  - 0 (Antibodies)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Chemokines)
RN  - 0 (Interleukin-1)
RN  - 0 (Interleukin-6)
RN  - 0 (Interleukin-8)
RN  - 0 (Recombinant Proteins)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 82115-62-6 (Interferon-gamma)
RN  - EC 3.4.21.5 (Thrombin)
SB  - IM
MH  - Antibodies/pharmacology
MH  - Cell Communication/*physiology
MH  - Chemokine CCL2/antagonists & inhibitors/metabolism
MH  - Chemokines/*metabolism
MH  - Coculture Techniques
MH  - Humans
MH  - Interferon-gamma/pharmacology
MH  - Interleukin-1/pharmacology
MH  - Interleukin-6/metabolism
MH  - Interleukin-8/antagonists & inhibitors/metabolism
MH  - Monocytes/*physiology
MH  - Pigment Epithelium of Eye/cytology/*physiology
MH  - Recombinant Proteins
MH  - Thrombin/*physiology
MH  - Tumor Necrosis Factor-alpha/biosynthesis/immunology/pharmacology
PMC - PMC1850462
EDAT- 2001/09/11 10:00
MHDA- 2001/10/12 10:01
PMCR- 2002/03/01
CRDT- 2001/09/11 10:00
PHST- 2001/09/11 10:00 [pubmed]
PHST- 2001/10/12 10:01 [medline]
PHST- 2001/09/11 10:00 [entrez]
PHST- 2002/03/01 00:00 [pmc-release]
AID - S0002-9440(10)61793-2 [pii]
AID - 2806 [pii]
AID - 10.1016/S0002-9440(10)61793-2 [doi]
PST - ppublish
SO  - Am J Pathol. 2001 Sep;159(3):1171-80. doi: 10.1016/S0002-9440(10)61793-2.