Key result
IL-1beta significantly increased the release of ET-1 from cultured human endometrial cells, an effect that was significantly attenuated by the nitric oxide synthase inhibitor LNMMA.
The NO/NOS system in human endometrium appears to be involved in regulating ET-1 release via IL-1beta secretion.
Hypothesis-generating for endometrial ET-1 regulation; no clinical implications from this Level 5 in vitro study.
The aim of this study was to investigate the influence of the nitric oxide/nitric oxide synthase (NO/NOS) system on the release of endothelin-1 (ET-1) in human endometrial cells. Human endometrial stromal cells in secretory phase were incubated for 72 h in serum-free RPMI 1640 medium in the absence or presence of different concentrations of interleukin-1beta (IL-1beta) and NG-monomethyl-L-arginine (LNMMA), a specific competitive inhibitor of NOS. ET-1 released from the cultured cells into the medium was determined by specific RIA. In all the experiments at various times, IL-1beta significantly increased the release of ET-1. LNMMA significantly attenuated the release of ET-1 when the cells were cultured with both IL-1beta and LNMMA, but LNMMA alone had no effect on ET-1 release. These results suggest that the NO/NOS system in human endometrium is involved in the regulation of ET-1 release via IL-1beta secretion. It can also be inferred that NO and ET-1 control the functions of endometrium in close association with IL-1beta.
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Kubota et al. (1998) studied Cultured human endometrial cells. Interleukin-1beta (IL-1beta) and NG-monomethyl-L-arginine (LNMMA) vs. Absence of IL-1beta and LNMMA was evaluated on Release of endothelin-1 (ET-1). IL-1beta significantly increased the release of ET-1 from cultured human endometrial cells, an effect that was significantly attenuated by the nitric oxide synthase inhibitor LNMMA.
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