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Amplification of Nitric Oxide Synthase Expression by Nitric Oxide in Interleukin 1β-Stimulated Rat Mesangial Cells

  • Heiko Mühl
  • Josef M. Pfeilschifter
Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 387)

Abstract

Nitric oxide (NO), a free-radical gas produced by many cell types, mediates blood vessel relaxation, functions as a neurotransmitter in the central and peripheral nervous system mediates macrophage cytotoxicity during host defence and leads to tissue injury in some inflammatory and autoimmune diseases. Increasing evidence indicates that NO orchestrates acute and chronic inflammatory processes and contributes to the pathomechanisms of septic shock, destruction of pancreatic islet cells during the development of insulin-dependent type 1 diabetes, adjuvant arthritis, progression of renal failure and neural destruction in vascular stroke and other neurodegenerative diseases (1). The careful control of this extremely reactive molecule is essential for the prevention of deleterious inflammatory reactions. Whereas the activity of the constitutive brain and endothelial cell NO synthases are mainly regulated posttranslationally by cytoplasmic Ca2+ levels or phosphorylation by a variety of protein kinases, the inducible NO synthase is regulated primarily at a transcriptional level. Once induced, the latter enzyme synthesizes NO for long periods of hours and days.

Keywords

Nitric Oxide Mesangial Cell Adjuvant Arthritis Nitrite Production Glomerular Mesangial Cell 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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Copyright information

© Springer Science+Business Media New York 1996

Authors and Affiliations

  1. 1.Department of PharmacologyBiozentrum, University of BaselBaselSwitzerland

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