Secretion of Monocyte Chemoattractant Protein-1 by Endothelial Cells of the Bovine Corpus Luteum: Regulation by Cytokines But Not Prostaglandin F2α

• Published in: Endocrinology (Philadelphia) Vol. 143; no. 9; pp. 3582 - 3589
• Main Authors: Cavicchio, Victoria A, Pru, James K, Davis, Benjamin S, Davis, John S, Rueda, Bo R, Townson, David H
• Format: Journal Article
• Language: English
• Published: Endocrine Society 01.09.2002
• ISSN: 0013-7227; 1945-7170
• DOI: 10.1210/en.2002-220388

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 F2α (PGF2α), and progesterone regulate MCP-1 expression. Endothelial cells were treated without (Control) or with PGF2α (1 μm), TNFα (100 ng/ml), interferon-γ (IFNγ, 200 IU/ml), and TNFα + IFNγ 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 TNFα within 24 and 48 h of culture, respectively (P < 0.05). Interferon-γ 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 TNFα + IFNγ lead to further increases (P < 0.05) in MCP-1 in both 24- and 48-h cultures. Surprisingly, neither PGF2α nor P4 affected MCP-1 production. Subsequent experiments revealed that the endothelial cells lacked prostaglandin F2α receptor mRNA, and the MAPK pathway, although present and responsive to growth factor stimulation, was unresponsive to PGF2α stimulation. In summary, endothelial cells derived from bovine CL respond to TNFα and IFNγ stimulation with an increase in MCP-1 secretion. In contrast, neither PGF2α nor P4 directly influenced endothelial expression of MCP-1. These results suggest that cytokines stimulate the synthesis of MCP-1 observed during PGF2α-induced luteal regression.