Abstract
Tumor necrosis factor α (TNFα) has been shown to be a potent stimulator of prostaglandin (PG) F(2α) secretion in the bovine endometrium. The aims of the present study were to determine the cell types in the endometrium (epithelial or stromal cells) responsible for the secretion of PGF(2α) in response to TNFα, and the intracellular mechanisms of TNFα action. Cultured bovine epithelial and stromal cells were exposed to TNFα (0.006-6 nM) or oxytocin (100 nM) for 4 h. TNFα resulted in a dose-dependent increase of PGF(2α) production in the stromal cells (P <0.001) but not in the epithelial cells. On the other hand, oxytocin stimulated PGF(2α) output in the epithelial cells but not in the stromal cells. When the stromal cells were incubated for 24 h with TNFα and inhibitors of phospholipase (PL) C or PLA2, only PLA2 inhibitor completely stopped the actions of TNFα (P <0.001). When the stromal cells were exposed to TNFα and arachidonic acid, the action of TNFα was augmented (P <0.001). When the stromal cells were incubated for 24 h with a nitric oxide (NO) donor (S-NAP), S-NAP stimulated the PGF(2α) production dose-dependently. Although an NO synthase (NOS) inhibitor (L-NAME) reduced TNFα-stimulated PGF(2α) production, an inhibitor of phosphodiesterase augmented the actions of TNFα and S-NAP (P <0.05). The overall results indicate that the target of TNFα for stimulation of PGF(2α) production in cattle is the endometrial stromal cells, and that the actions of TNFα are mediated via the activation of PLA2 and arachidonic acid conversion. Moreover, TNFα may exert a stimulatory effect on PGF(2α) production via the induction of NOS and the subsequent NO-cGMP formation.
| Original language | English |
|---|---|
| Pages (from-to) | 1116-1120 |
| Number of pages | 5 |
| Journal | Biology of Reproduction |
| Volume | 62 |
| Issue number | 5 |
| Publication status | Published - 2000 |
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ASJC Scopus subject areas
- Cell Biology
- Developmental Biology
- Embryology
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Production of prostaglandin F(2α) by cultured bovine endometrial cells in response to tumor necrosis factor α : Cell type specificity and intracellular mechanisms. / Skarzynski, Dariusz J.; Miyamoto, Yoko; Okuda, Kiyoshi.
In: Biology of Reproduction, Vol. 62, No. 5, 2000, p. 1116-1120.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Production of prostaglandin F(2α) by cultured bovine endometrial cells in response to tumor necrosis factor α
T2 - Cell type specificity and intracellular mechanisms
AU - Skarzynski, Dariusz J.
AU - Miyamoto, Yoko
AU - Okuda, Kiyoshi
PY - 2000
Y1 - 2000
N2 - Tumor necrosis factor α (TNFα) has been shown to be a potent stimulator of prostaglandin (PG) F(2α) secretion in the bovine endometrium. The aims of the present study were to determine the cell types in the endometrium (epithelial or stromal cells) responsible for the secretion of PGF(2α) in response to TNFα, and the intracellular mechanisms of TNFα action. Cultured bovine epithelial and stromal cells were exposed to TNFα (0.006-6 nM) or oxytocin (100 nM) for 4 h. TNFα resulted in a dose-dependent increase of PGF(2α) production in the stromal cells (P <0.001) but not in the epithelial cells. On the other hand, oxytocin stimulated PGF(2α) output in the epithelial cells but not in the stromal cells. When the stromal cells were incubated for 24 h with TNFα and inhibitors of phospholipase (PL) C or PLA2, only PLA2 inhibitor completely stopped the actions of TNFα (P <0.001). When the stromal cells were exposed to TNFα and arachidonic acid, the action of TNFα was augmented (P <0.001). When the stromal cells were incubated for 24 h with a nitric oxide (NO) donor (S-NAP), S-NAP stimulated the PGF(2α) production dose-dependently. Although an NO synthase (NOS) inhibitor (L-NAME) reduced TNFα-stimulated PGF(2α) production, an inhibitor of phosphodiesterase augmented the actions of TNFα and S-NAP (P <0.05). The overall results indicate that the target of TNFα for stimulation of PGF(2α) production in cattle is the endometrial stromal cells, and that the actions of TNFα are mediated via the activation of PLA2 and arachidonic acid conversion. Moreover, TNFα may exert a stimulatory effect on PGF(2α) production via the induction of NOS and the subsequent NO-cGMP formation.
AB - Tumor necrosis factor α (TNFα) has been shown to be a potent stimulator of prostaglandin (PG) F(2α) secretion in the bovine endometrium. The aims of the present study were to determine the cell types in the endometrium (epithelial or stromal cells) responsible for the secretion of PGF(2α) in response to TNFα, and the intracellular mechanisms of TNFα action. Cultured bovine epithelial and stromal cells were exposed to TNFα (0.006-6 nM) or oxytocin (100 nM) for 4 h. TNFα resulted in a dose-dependent increase of PGF(2α) production in the stromal cells (P <0.001) but not in the epithelial cells. On the other hand, oxytocin stimulated PGF(2α) output in the epithelial cells but not in the stromal cells. When the stromal cells were incubated for 24 h with TNFα and inhibitors of phospholipase (PL) C or PLA2, only PLA2 inhibitor completely stopped the actions of TNFα (P <0.001). When the stromal cells were exposed to TNFα and arachidonic acid, the action of TNFα was augmented (P <0.001). When the stromal cells were incubated for 24 h with a nitric oxide (NO) donor (S-NAP), S-NAP stimulated the PGF(2α) production dose-dependently. Although an NO synthase (NOS) inhibitor (L-NAME) reduced TNFα-stimulated PGF(2α) production, an inhibitor of phosphodiesterase augmented the actions of TNFα and S-NAP (P <0.05). The overall results indicate that the target of TNFα for stimulation of PGF(2α) production in cattle is the endometrial stromal cells, and that the actions of TNFα are mediated via the activation of PLA2 and arachidonic acid conversion. Moreover, TNFα may exert a stimulatory effect on PGF(2α) production via the induction of NOS and the subsequent NO-cGMP formation.
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UR - http://www.scopus.com/inward/citedby.url?scp=0034095012&partnerID=8YFLogxK
M3 - Article
C2 - 10775156
AN - SCOPUS:0034095012
VL - 62
SP - 1116
EP - 1120
JO - Biology of Reproduction
JF - Biology of Reproduction
SN - 0006-3363
IS - 5
ER -