Key result
In cultured vascular smooth muscle cells, prolonged activation of soluble guanylyl cyclase by NO down-regulates PKG expression, while loss of PKG expression increases sGC expression.
Population
Vascular smooth muscle cells including freshly isolated non-passaged bovine aortic SMC, passaged bovine…
Comparison
Pro-inflammatory cytokines, NO donors, and… vs Untreated cells or baseline expression states
Design
Preclinical
Follow-up
48 h (for NO donor treatment)
Authors
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Suggests feedback regulation in NO-sGC-PKG signaling in VSMCs; leaves open in vivo relevance and clinical implications.
There is a coordinated regulatory mechanism in vascular smooth muscle cells where prolonged sGC activation down-regulates PKG expression, and loss of PKG increases sGC expression.
Browner et al. (2004) studied this question. Adenovirus encoding sGC subunits and NO donors vs. Untreated or non-transduced cells was evaluated on PKG and sGC protein expression. In cultured vascular smooth muscle cells, prolonged activation of soluble guanylyl cyclase by NO down-regulates PKG expression, while loss of PKG expression increases sGC expression.
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