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Just as studies have demonstrated that SA produces NO, it is also possible that NO stimulates SA accumulation [ 32, 33].
The reporter gene expression was significantly stimulated by NO donor, suggesting that NO stimulates antioxidant genes through the cis-acting ARE DNA sequences.
Our data indicate that NO stimulates CXCR4 expression in vitro.
In addition, oxidative stress caused by NO stimulates satellite cell proliferation [ 29], a process essential for muscle regeneration.
Like L-arginine, SNP was also able to enhance insulin secretion (Fig. 2B), indicating that production of NO stimulates insulin secretion.
For instance, studies in vitro have shown that NO stimulates secretion of gastric acid in the mouse[ 17, 18] and bullfrog[ 19].
Similar(44)
Conversely, suppressing CD47 expression in Jurkat T-cells using a CD47-specific morpholino abolished the effect of Aβ on NO-stimulated cGMP accumulation (Fig. 4B).
Not investigated in this study were mediators of the NO-stimulated invasion, which lead to essential steps as migration and matrix degradation.
NO also stimulates MMP production and activity in osteoarthritic joint cartilage [50].
Particularly, IL-1β produces PGE2 and NO, and stimulates the expression of other inflammatory cytokines and MMPs [ 27].
4E-BP prevents formation of the translation initiation complex eIF4F, thereby inhibiting m7G-dependent trandlation, and S6K no longer stimulates eIF4A.
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