PMID- 1733731
OWN - NLM
STAT- MEDLINE
DCOM- 19920303
LR  - 20131121
IS  - 0013-7227 (Print)
IS  - 0013-7227 (Linking)
VI  - 130
IP  - 2
DP  - 1992 Feb
TI  - Tumor necrosis factor-alpha alters bovine luteal cell synthetic capacity and 
      viability.
PG  - 854-60
AB  - Tumor necrosis factor-alpha (TNF-alpha) is a macrophage-derived cytokine that is 
      also reportedly produced by granulosal cells and is localized in luteal cells. 
      The present study employed serum-free culture of midcycle bovine luteal cells to 
      investigate the effects of TNF-alpha, alone and with other cytokines, on luteal 
      function. TNF-alpha (1-1000 ng/ml) produced a dose-dependent increase in 
      prostaglandin (PG)F2 alpha and 6-keto-PGF1 alpha synthesis on all days of 
      culture, but had no effect on basal progesterone (P4) production. TNF-alpha, in 
      combination with other known stimulators of luteal PG synthesis, interleukin-1 
      beta (2.5 ng/ml) or interferon-gamma (IFN-gamma, 100 U/ml), had synergistic 
      effects on PGF2 alpha production (greater than 50-fold above control, P less than 
      0.05) whereas interferon-alpha (1000 U/ml) significantly suppressed 
      TNF-alpha-stimulated PGF2 alpha production. By day 7 of culture, TNF-alpha 
      inhibited LH-stimulated P4 production (P less than 0.05). Luteal cell numbers 
      were significantly reduced by IFN-gamma but not by TNF-alpha alone. However, the 
      combination of TNF-alpha + IFN-gamma was extremely cytotoxic (only 20% of cells 
      maintained as compared to control). Finally, TNF-alpha (100 ng/ml) enhanced the 
      expression of Class I major histocompatibility complex antigens on cultured 
      bovine luteal cells but did not alter IFN-gamma induction of Class II major 
      histocompatibility complex antigens. In light of these findings, it appears that 
      TNF-alpha, in conjunction with other cytokines, is a modulator of luteal cell 
      function in vitro. The stimulation of PG synthesis, as well as cytotoxic effects 
      of TNF-alpha, may suggest a role in luteolysis.
FAU - Benyo, D F
AU  - Benyo DF
AD  - Department of Dairy Science, Ohio State University, Columbus 43210.
FAU - Pate, J L
AU  - Pate JL
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PT  - Research Support, U.S. Gov't, Non-P.H.S.
PL  - United States
TA  - Endocrinology
JT  - Endocrinology
JID - 0375040
RN  - 0 (Interleukin-1)
RN  - 0 (Recombinant Proteins)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 4G7DS2Q64Y (Progesterone)
RN  - 58962-34-8 (6-Ketoprostaglandin F1 alpha)
RN  - 82115-62-6 (Interferon-gamma)
RN  - B7IN85G1HY (Dinoprost)
SB  - IM
MH  - 6-Ketoprostaglandin F1 alpha/*metabolism
MH  - Animals
MH  - Cattle
MH  - Cell Survival/drug effects
MH  - Cells, Cultured
MH  - Corpus Luteum/cytology/*drug effects/metabolism
MH  - Dinoprost/*metabolism
MH  - Dose-Response Relationship, Drug
MH  - Drug Interactions
MH  - Female
MH  - Humans
MH  - Interferon-gamma/pharmacology
MH  - Interleukin-1/pharmacology
MH  - Kinetics
MH  - Progesterone/*metabolism
MH  - Radioimmunoassay
MH  - Recombinant Proteins/pharmacology
MH  - Tumor Necrosis Factor-alpha/*pharmacology
EDAT- 1992/02/01 00:00
MHDA- 1992/02/01 00:01
CRDT- 1992/02/01 00:00
PHST- 1992/02/01 00:00 [pubmed]
PHST- 1992/02/01 00:01 [medline]
PHST- 1992/02/01 00:00 [entrez]
AID - 10.1210/endo.130.2.1733731 [doi]
PST - ppublish
SO  - Endocrinology. 1992 Feb;130(2):854-60. doi: 10.1210/endo.130.2.1733731.