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Secretion of Monocyte Chemoattractant Protein-1 by Endothelial Cells of the Bovine Corpus Luteum: Regulation by Cytokines But Not Prostaglandin F2

Department of Animal and Nutritional Sciences (V.A.C., D.H.T.), University of New Hampshire-Durham, Durham, New Hampshire 03824; Vincent Center for Reproductive Biology (B.R.R., J.K.P.), Massachusetts General Hospital/Harvard Medical School, Boston, Massachusetts 02114; Women’s Research Institute (B.S.D., J.S.D.), University of Kansas School of Medicine-Wichita, Veterans Affairs Medical Center, Wichita, Kansas 67214; and Olson Center for Women’s Health (J.S.D.), Department of Obstetrics and Gynecology, University of Nebraska Medical Center, Omaha, Nebraska 68198

Address all correspondence and requests for reprints to: David H. Townson, Ph.D., Department of Animal and Nutritional Sciences, University of New Hampshire, 128 Main Street, Durham, New Hampshire 03824. E-mail: dave.townson{at}unh.edu.

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 F2 (PGF2), and progesterone regulate MCP-1 expression. Endothelial cells were treated without (Control) or with PGF2 (1 µM), TNF (100 ng/ml), interferon- (IFN, 200 IU/ml), and TNF + IFN 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 TNF within 24 and 48 h of culture, respectively (P < 0.05). Interferon- 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 TNF + IFN lead to further increases (P < 0.05) in MCP-1 in both 24- and 48-h cultures. Surprisingly, neither PGF2 nor P4 affected MCP-1 production. Subsequent experiments revealed that the endothelial cells lacked prostaglandin F2 receptor mRNA, and the MAPK pathway, although present and responsive to growth factor stimulation, was unresponsive to PGF2 stimulation. In summary, endothelial cells derived from bovine CL respond to TNF and IFN stimulation with an increase in MCP-1 secretion. In contrast, neither PGF2 nor P4 directly influenced endothelial expression of MCP-1. These results suggest that cytokines stimulate the synthesis of MCP-1 observed during PGF2-induced luteal regression.

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