Nitric oxide mediates interleukin-1-induced prostaglandin E2 production by vascular smooth muscle cells.

@article{Inoue1993NitricOM,
  title={Nitric oxide mediates interleukin-1-induced prostaglandin E2 production by vascular smooth muscle cells.},
  author={T. Inoue and K. Fukuo and S. Morimoto and E. Koh and T. Ogihara},
  journal={Biochemical and biophysical research communications},
  year={1993},
  volume={194 1},
  pages={
          420-4
        }
}
We examined the possible participation of nitric oxide (NO) in the activation of cyclooxygenase, a heme-containing enzyme, induced by interleukin-1 (IL-1) in vascular smooth muscle cells (VSMC). IL-1 induced a delayed and prolonged release of both NO and prostaglandin E2 (PGE2) from VSMC. NG-monomethyl-L-arginine (L-NMMA), an inhibitor of NO synthesis, partially but significantly inhibited the PGE2 release induced by IL-1, whereas it completely inhibited the IL-1-induced NO production. The… Expand
Phospholipase A2 metabolites regulate inducible nitric oxide synthase in myocytes.
TLDR
Data suggest that: (1) IL upregulates COX-2 expression and prostanoid production in NVM; and (2) AA metabolites other than COX products, possibly products of the LO pathway, are involved in IL regulation of iNOS. Expand
Endothelin-1 enhances nitric oxide-induced cytotoxicity in vascular smooth muscle.
TLDR
Findings suggest that endothelin-1 secreted from endothelial cells may enhance nitric oxide-induced cytotoxicity by means of the ETA receptor in vascular smooth muscle cells. Expand
Nitric oxide enhances PGI(2)production by human pulmonary artery smooth muscle cells.
TLDR
Exogenous NO together with endogenous NO induced by LPS or cytokines from smooth muscle cells might synergetically enhance PGI(2)production by these cells, possibly in clinical disorders such as sepsis and acute respiratory distress syndrome. Expand
Functional and cellular interactions between nitric oxide and prostacyclin
TLDR
It is suggested that NO, through cGMP-dependent protein kinases, produces the phosphorylation of a 104-kDa protein that is associated with inhibition in the activity of the COX-I, decreasing PGI, synthesis and thereby decreasing coronary. Expand
cGMP upregulates nitric oxide synthase expression in vascular smooth muscle cells.
TLDR
8-Br-cGMP enhanced the interleukin-1-induced increase in tumor necrosis factor-alpha messenger RNA level in vascular smooth muscle cells, indicating that cGMP may upregulate inducible nitric oxide synthase gene expression through the stimulation of tumor Necrosis Factor-alpha production in vascular smoother muscle cells. Expand
Dual inhibition of nitric oxide and prostaglandin production contributes to the antiinflammatory properties of nitric oxide synthase inhibitors.
We have recently put forward the hypothesis that the dual inhibition of proinflammatory nitric oxide (NO) and prostaglandins (PG) may contribute to the antiinflammatory properties of nitric oxideExpand
Inducible nitric oxide synthase mediates prostaglandin h2 synthase nitration and suppresses eicosanoid production.
TLDR
It is shown that inducible NO synthase (iNOS) and PGHS-1 co-localize in atherosclerotic lesions of ApoE(-/-) mouse aortae, and a regulatory role of iNOS in eicosanoid biosynthesis in human atherosclerosis lesions is suggested. Expand
Inducible nitric oxide synthase expression in activated rat microglial cultures is downregulated by exogenous prostaglandin E2 and by cyclooxygenase inhibitors
TLDR
Exogenous prostaglandin E2 (PGE2), which is known to increase cyclic adenosine monophosphate (cAMP) levels in microglial cells, downregulates LPS‐induced iNOS expression in a dose‐dependent manner, suggesting a positive modulatory effect of endogenous prostanoids of iN OS expression, as opposed to the inhibitory effect of exogenous PGE2. Expand
Functional and cellular interactions between nitric oxide and prostacyclin.
TLDR
It is suggested that NO, through cGMP-dependent protein kinases, produces the phosphorylation of a 104-kDa protein that is associated with inhibition in the activity of the COX-1, decreasing P GI(2) synthesis and thereby decreasing coronary PGI(2)-mediated vasodilatation. Expand
Release of isoprostanes by human pulmonary artery in organ culture: a cyclo-oxygenase and nitric oxide dependent pathway.
TLDR
It is shown for the first time that human pulmonary vessels can produce isporostanes and that NO synthase and cyclo-oxygenase pathways are involved in their release. Expand
...
1
2
3
4
5
...