PMID- 12193574
OWN - NLM
STAT- MEDLINE
DCOM- 20020923
LR  - 20181130
IS  - 0013-7227 (Print)
IS  - 0013-7227 (Linking)
VI  - 143
IP  - 9
DP  - 2002 Sep
TI  - Secretion of monocyte chemoattractant protein-1 by endothelial cells of the 
      bovine corpus luteum: regulation by cytokines but not prostaglandin F2alpha.
PG  - 3582-9
AB  - Information regarding the regulation of monocyte chemoattractant protein-1 
      (MCP-1) in regression of the corpus luteum (CL) is limited. This study tested the 
      hypothesis that endothelial cells derived from bovine CL are a source of MCP-1, 
      and that proinflammatory cytokines, prostaglandin F2alpha (PGF2alpha), and 
      progesterone regulate MCP-1 expression. Endothelial cells were treated without 
      (Control) or with PGF2alpha (1 micro M), TNFalpha (100 ng/ml), interferon-gamma 
      (IFNgamma, 200 IU/ml), and TNFalpha + IFNgamma for 24 and 48 h in the absence or 
      presence of progesterone (P4, 250 ng/ml). Increases in MCP-1 mRNA and protein 
      were observed in response to TNFalpha within 24 and 48 h of culture, respectively 
      (P < 0.05). Interferon-gamma stimulated (P < 0.05) both MCP-1 mRNA and protein 
      after 24 h of culture, and this effect was also sustained through 48 h of culture 
      (P < 0.05). Cotreatment of cultures with TNFalpha + IFNgamma lead to further 
      increases (P < 0.05) in MCP-1 in both 24- and 48-h cultures. Surprisingly, 
      neither PGF2alpha nor P4 affected MCP-1 production. Subsequent experiments 
      revealed that the endothelial cells lacked prostaglandin F2alpha receptor mRNA, 
      and the MAPK pathway, although present and responsive to growth factor 
      stimulation, was unresponsive to PGF2alpha stimulation. In summary, endothelial 
      cells derived from bovine CL respond to TNFalpha and IFNgamma stimulation with an 
      increase in MCP-1 secretion. In contrast, neither PGF2alpha nor P4 directly 
      influenced endothelial expression of MCP-1. These results suggest that cytokines 
      stimulate the synthesis of MCP-1 observed during PGF2alpha-induced luteal 
      regression.
FAU - Cavicchio, Victoria A
AU  - Cavicchio VA
AD  - Department of Animal and Nutritional Sciences, University of New 
      Hampshire-Durham, Durham, New Hampshire 03824, USA.
FAU - Pru, James K
AU  - Pru JK
FAU - Davis, Benjamin S
AU  - Davis BS
FAU - Davis, John S
AU  - Davis JS
FAU - Rueda, Bo R
AU  - Rueda BR
FAU - Townson, David H
AU  - Townson DH
LA  - eng
GR  - R01-HD-35934/HD/NICHD NIH HHS/United States
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PT  - Research Support, U.S. Gov't, P.H.S.
PL  - United States
TA  - Endocrinology
JT  - Endocrinology
JID - 0375040
RN  - 0 (3,3'-dihexadecylindocarbocyanine)
RN  - 0 (Carbocyanines)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Cytokines)
RN  - 0 (Fluorescent Dyes)
RN  - 0 (Lipoproteins, LDL)
RN  - 0 (RNA, Messenger)
RN  - 0 (Receptors, Prostaglandin)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 0 (acetyl-LDL)
RN  - 0 (prostaglandin F2alpha receptor)
RN  - 4G7DS2Q64Y (Progesterone)
RN  - 82115-62-6 (Interferon-gamma)
RN  - B7IN85G1HY (Dinoprost)
RN  - EC 2.7.11.24 (Mitogen-Activated Protein Kinases)
SB  - IM
MH  - Animals
MH  - Carbocyanines
MH  - Cattle
MH  - Chemokine CCL2/genetics/*metabolism
MH  - Corpus Luteum/*blood supply
MH  - Cytokines/*pharmacology
MH  - Dinoprost/*pharmacology
MH  - Endothelium, Vascular/chemistry/*metabolism
MH  - Female
MH  - Fluorescent Dyes
MH  - Gene Expression Regulation/*drug effects
MH  - Interferon-gamma/pharmacology
MH  - Lipoproteins, LDL/metabolism
MH  - Mitogen-Activated Protein Kinases/metabolism
MH  - Phosphorylation
MH  - Progesterone/pharmacology
MH  - RNA, Messenger/analysis
MH  - Receptors, Prostaglandin/analysis
MH  - Tumor Necrosis Factor-alpha/pharmacology
EDAT- 2002/08/24 10:00
MHDA- 2002/09/24 06:00
CRDT- 2002/08/24 10:00
PHST- 2002/08/24 10:00 [pubmed]
PHST- 2002/09/24 06:00 [medline]
PHST- 2002/08/24 10:00 [entrez]
AID - 10.1210/en.2002-220388 [doi]
PST - ppublish
SO  - Endocrinology. 2002 Sep;143(9):3582-9. doi: 10.1210/en.2002-220388.