Document Detail

Cytokine regulation of inducible nitric oxide synthase in vascular smooth muscle cells.
MedLine Citation:
PMID:  9575557     Owner:  NLM     Status:  MEDLINE    
NO is an important mediator in sepsis. It has been unequivocally established that it is the major determinant in the vasodilatation and consequent hypotension in experimental animals following the administration of LPS. It is cytotoxic, particularly in combination with superoxide anions, and exerts negative inotropic and chronotropic effects on the heart. The exact role that these functions play in sepsis, however, remain unclear. Similarly, its immunomodulatory and cerebral effects, although potentially important, remain of uncertain significance in sepsis. Regulation of such a pivotal molecule is clearly extremely important: the data described here show that not only is this regulation extremely complex, but it appears to vary in different cell types. The implication of this finding for future clinical work is clear. NO production is not all bad: in some circumstances, it may be desirable to differentially regulate iNOS activity such that production is restricted in some cell types but not in others. The work described here begins to offer the possibility of identifying new molecular targets which allow this kind of differential regulation.
J Cohen; T J Evans; J Spink
Related Documents :
17601517 - Silencing of caspase-8 and caspase-3 by rna interference prevents vascular endothelial ...
14960967 - Burn injury and pulmonary sepsis: development of a clinically relevant model.
20954877 - Immunomodulatory cell therapy in sepsis: have we learnt lessons from the past?
17380787 - Blockade of apoptosis as a rational therapeutic strategy for the treatment of sepsis.
24631687 - Ocilrp2 signaling synergizes with lps to induce the maturation and differentiation of m...
17991287 - Shift of c3 deposition from localization in the glomerulus into the tubulo-interstitial...
Publication Detail:
Type:  Journal Article; Review    
Journal Detail:
Title:  Progress in clinical and biological research     Volume:  397     ISSN:  0361-7742     ISO Abbreviation:  Prog. Clin. Biol. Res.     Publication Date:  1998  
Date Detail:
Created Date:  1998-07-10     Completed Date:  1998-07-10     Revised Date:  2011-10-27    
Medline Journal Info:
Nlm Unique ID:  7605701     Medline TA:  Prog Clin Biol Res     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  169-77     Citation Subset:  IM    
Department of Infectious Diseases, Royal Postgraduate Medical School, Hammersmith Hospital, London, United Kingdom.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Cytokines / physiology*
Enzyme Activation
Enzyme Induction
Gene Expression Regulation, Enzymologic
Muscle, Smooth, Vascular / enzymology*
Nitric Oxide Synthase / biosynthesis*,  genetics
Nitric Oxide Synthase Type II
Reg. No./Substance:
0/Cytokines; EC protein, human; EC Oxide Synthase; EC Oxide Synthase Type II

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

Previous Document:  ADP-ribosylation: role in LPS-induced phosphorylation of two cytosolic proteins (p36/38) in monocyte...
Next Document:  Antibiotic-mediated release of endotoxin and the pathogenesis of gram-negative sepsis.