Publication: Molecular actions of nitric oxide in mesangial cells
Authors
Sandau, K.B. ; Brune, B.
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Publisher
Murcia : F. Hernández
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DOI
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info:eu-repo/semantics/article
Description
Abstract
Nitric oxide (NO) is a widely recognized
mediator of physiological and pathophysiological signal
transmission. Its generation through L-arginine
metabolism is relevant in the mesangium of the kidney
where NO is produced by constitutive and inducible NOsynthase
isoenzymes. Signaling is achieved through
target interactions via redox and additive chemistry. In
mesangial cells (MC), the outcome of these
modifications promote on one side activation of soluble
guanylyl cyclase while on the other side cytotoxicity is
elicited. These contrasting situations are characterized
by: 1) cGMP formation and signal propagation towards
myosin light chain kinase, the effector system that
regulates F-actin assembly, thereby affecting reversible
relaxation/contraction of mesangial cells; and 2)
initiation of morphological and biochemical alterations
that are reminiscent of apoptosis such as chromatin
condensation, p53 or Bax accumulation as well as
caspase-3 activation. Off note, NO formation with
concomitant initiation of apoptosis is efficiently
antagonized by the simultaneous presence of superoxide
(02-). We will recall the consequences that stem from a
diffusion controlled NO/02- interaction thereby
redirecting the apoptotic initiating activity of either NO
or 02- towards protection. The crosstalk between cell
destructive and protective signaling pathways, their
activation or inhibition under the modulatory influence
of NO will be discussed. Here we give examples of how
NO elicits physiological and pathophysiological signal
transmission in rat MC.
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