Possible involvement of tyrosine kinase activation in lipopolysaccharide-induced expression of Ca(2+)-insensitive but calmodulin-coupling nitric oxide synthase in rat glial cells

J Neurosci Res. 1996 Jan 15;43(2):235-45. doi: 10.1002/(SICI)1097-4547(19960115)43:2<235::AID-JNR11>3.0.CO;2-5.

Abstract

To clarify the properties of an inducible type of nitric oxide synthase (i-NOS) in the brain, we examined whether lipopolysaccharide (LPS) induces NOS in glial cells cultured from neonatal rats. NOS activities (NO2- accumulation and L-[14C]citrulline formation) were detected by treatment with LPS at 10 micrograms/ml for 6-72 hr. L-[14C]citrulline formation by LPS-induced i-NOS was inhibited by NG-monomethyl-L-arginine (a NOS inhibitor) and diphenyleneiodonium (a flavo-protein inhibitor). The activity was not markedly changed in the presence or absence of Ca2+. The induction of i-NOS by LPS was abolished by cycloheximide, actinomycin D, or dexamethasone. In addition, the induction was inhibited by herbimycin A (a tyrosine kinase inhibitor), but was not by staurosporine, W-7, or FK-506. After LPS stimulation, 130 kDa proteins were reacted with anti-rat liver i-NOS antibody 5-72 hr. i-NOS induced from glial cells coupled tightly with endogenous calmodulin (CaM) even in the absence of Ca2+. These results suggest that LPS induces expression of 130-kDa i-NOS through an activation of tyrosine kinase, after which i-NOS couples with CaM, and that NO is formed for 6-72 hr in glial cells.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Calcium / pharmacology
  • Calmodulin / metabolism*
  • Cells, Cultured
  • Citrulline / metabolism
  • Endotoxins / pharmacology
  • Enzyme Activation / drug effects
  • Enzyme Inhibitors / pharmacology
  • Escherichia coli / metabolism
  • Immunohistochemistry
  • Lipopolysaccharides / pharmacology*
  • Male
  • Neuroglia / drug effects
  • Neuroglia / enzymology*
  • Nitric Oxide / metabolism
  • Nitric Oxide Synthase / antagonists & inhibitors
  • Nitric Oxide Synthase / metabolism*
  • Nitroarginine / pharmacology
  • Protein-Tyrosine Kinases / antagonists & inhibitors
  • Protein-Tyrosine Kinases / metabolism*
  • Rats
  • Rats, Wistar

Substances

  • Calmodulin
  • Endotoxins
  • Enzyme Inhibitors
  • Lipopolysaccharides
  • Nitroarginine
  • Citrulline
  • Nitric Oxide
  • endotoxin, Escherichia coli
  • Nitric Oxide Synthase
  • Protein-Tyrosine Kinases
  • Calcium