Inhibition of Inducible Nitric Oxide Synthase Expression by Endothelin in Rat Glial Cells Prepared from the Neonatal Rat Brain

Oda, Haruko; Murayama, Toshihiko; Nomura, Yasuyuki

doi:10.1046/j.1471-4159.1997.69020669.x

Cited by 23 publications

(4 citation statements)

References 22 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…In addition, a growing body of evidence proposes that nitric oxide is also involved in the development of morphine tolerance, dependence, and withdrawal . Researchers have proven that in primary cultured rat glial cells, bucladesine and other cAMP‐elevating agents could inhibit inducible NO synthase (iNOS) and NO accumulation . Decrease in the expression or deletion of the iNOS gene reduced peripheral morphine tolerance .…”

Section: Discussionmentioning

confidence: 99%

Dual effect of cAMP agonist on ameliorative function of PKA inhibitor in morphine‐dependent mice

Seyedi

Salehi

Payandemehr

et al. 2013

Fundamemntal Clinical Pharma

View full text Add to dashboard Cite

The present study shows interactive effects of bucladesine (db-cAMP) as a cyclic adenosine monophosphate (cAMP) agonist and H-89 as a protein kinase A (PKA) inhibitor on naloxone-induced withdrawal signs in morphine-dependent mice. Animals were treated subcutaneously with morphine thrice daily with doses progressively increased from 50 to 125 mg/kg. A last dose of morphine (50 mg/kg) was administered on the 4th day. Several withdrawal signs were precipitated by intraperitoneal (i.p.) administration of naloxone (5 mg/kg). Different doses of bucladesine (50, 100, 200 nm/mouse) and H-89 (0.05, 0.5, 1, 5 mg/kg) were administered (i.p.) 60 min before naloxone injection. In combination groups, bucladesine was injected 15 min before H-89 injection. Single administration of H-89 (0.5, 1, 5 mg/kg) and bucladesine (50, 100 nm/mouse) significantly attenuated prominent behavioral signs of morphine withdrawal. Lower doses of bucladesine (50, 100 nm/mouse) in combination with H-89 (0.05 mg/kg) increased the inhibitory effects of H-89 on withdrawal signs while in high dose (200 nm/mouse) decreased the ameliorative function of H-89 (0.05 mg/kg) in morphine-dependent animals. It is concluded that H-89 and bucladesine could affect morphine withdrawal syndrome via possible interaction with cyclic nucleotide messengering systems, protein kinase A signaling pathways, and modified related neurotransmitters.

show abstract

Section: Discussionmentioning

confidence: 99%

Dual effect of cAMP agonist on ameliorative function of PKA inhibitor in morphine‐dependent mice

Seyedi

Salehi

Payandemehr

et al. 2013

Fundamemntal Clinical Pharma

View full text Add to dashboard Cite

show abstract

“…1993; Feinstein 1998). Suppression of glial cell NOS2 expression by other agents which increase cAMP has also been described (Oda et al . 1997; Pahan et al .…”

mentioning

confidence: 82%

A 27‐bp region of the inducible nitric oxide synthase promoter regulates expression in glial cells

Gavrilyuk¹,

Horváth²,

Weinberg³

et al. 2001

Journal of Neurochemistry

View full text Add to dashboard Cite

The expression of inducible nitric oxide synthase (NOS2) in glial cells is inhibited by neurotransmitters such as norepinephrine (NE) which elevate cAMP levels. We examined the molecular basis for this effect using a 2.2-kb fragment of the rat NOS2 promoter transfected into rat C6 glioma cells. Promoter activation (up to six-fold) by lipopolysaccharide (LPS) and interferon-g (IFNg) was reduced by NE, which alone had no effect. However, a promoter construct extending to bp 2130 and containing the proximal nuclear factor-kappa B (NF-kB) binding site was minimally activated by LPS and cytokines, but activated up to three-fold by NE. Deletion analysis identi®ed a 27-bp region (bp 2187 to 2160) as critical for mediating this suppressive effect. This region also enhanced promoter activation by LPS and cytokines, and prevented activation by NE alone. Gel shift analysis revealed constitutive binding to this region, and induction by NE of additional complexes which could be blocked by an antibody against CREB. NE also increased levels of the IkBa protein which could contribute to its suppressive effects. These results identify a critical role for this 27-bp region in regulation of NOS2 promoter activation and suppression by cAMP.

show abstract

“…These findings suggest that ETs may cause their harmful effects in bacterial meningitis through NO production. 35 A recent study showed that ET contributed to increases in CBF, intracranial pressure, brain water content, and CSF pleocytosis in adult rats with early pneumococcal meningitis. In vitro, stimulation of cerebral microvascular endothelial cells by pneumococci induced an increase in ET and NO concentrations.…”

Section: Discussionmentioning

confidence: 99%

Endothelin inhibition improves cerebral blood flow and is neuroprotective in pneumococcal meningitis

Pfister¹,

Tureen

Shaw

et al. 2000

Ann Neurol.

View full text Add to dashboard Cite

By using an infant rat model of pneumococcal meningitis, we determined whether endothelins contribute to neuronal damage in this disease. Cerebrospinal fluid analysis demonstrated a significant increase of endothelin‐1 in infected animals compared with uninfected controls. Histopathological examination 24 hours after infection showed brain damage in animals treated with ceftriaxone alone (median, 9.2% of cortex; range, 0–49.1%). In infected animals treated intraperitoneally with the endothelin antagonist bosentan (30 mg/kg, every 12 hours) also, injury was reduced to 0.5% (range, 0–8.6%) of cortex. Cerebral blood flow was reduced in infected animals (6.5 ± 4.0 ml/min/100 g of brain vs 14.9 ± 9.1 ml/min/100 g in controls. Treatment with bosentan restored cerebral blood flow to levels similar to controls (12.8 ± 5.3 ml/min/100 g). Improved blood flow was not mediated by nitric oxide production, because bosentan had no effect on cerebrospinal fluid or plasma nitrite/nitrate concentrations at 6, 12, or 18 hours. These data indicate that endothelins contribute to neuronal injury in this model of pneumococcal meningitis by causing cerebral ischemia. Ann Neurol 2000;47:329–335

show abstract

Inhibition of Inducible Nitric Oxide Synthase Expression by Endothelin in Rat Glial Cells Prepared from the Neonatal Rat Brain

Cited by 23 publications

References 22 publications

Dual effect of cAMP agonist on ameliorative function of PKA inhibitor in morphine‐dependent mice

Dual effect of cAMP agonist on ameliorative function of PKA inhibitor in morphine‐dependent mice

A 27‐bp region of the inducible nitric oxide synthase promoter regulates expression in glial cells

Endothelin inhibition improves cerebral blood flow and is neuroprotective in pneumococcal meningitis

Contact Info

Product

Resources

About