Sandbox Reserved 474: Difference between revisions

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== Mediator of Atherosclerosis ==

It has been shown that at known concentrations, CRP elicits effects which result in either proinflammatory or proatherosclerotic phenotype [4]. Several in vitro experiments have shown CRP to downregulate eNOS transcription, thus destabilizing its mRNA, resulting in in a decreased release of basel and stimulated NO, key endothelial factors [4]. By inhibiting NO production, CRP effectively facilitates apoptosis and blocks angiogenesis. Furthermore, it has been proposed that it is responsible for promoting the upregulation of nuclear factor-κB, which is a key promotor of several proatherosclerotic genes [4]. In addition, recent evidence has shown that it also has proatherogenic effects within smooth vascular muscle as well [1].

It has been shown that at known concentrations, CRP elicits effects which result in either proinflammatory or proatherosclerotic phenotype [4]. Several in vitro experiments have shown CRP to downregulate eNOS transcription, thus destabilizing its mRNA, resulting in in a decreased release of basel and stimulated NO, key endothelial factors [4]. By inhibiting NO production, CRP effectively facilitates apoptosis and blocks angiogenesis. Furthermore, it has been proposed that it is responsible for promoting the upregulation of nuclear factor-κB, which is a key promotor of several proatherosclerotic genes [4]. In addition, recent evidence has shown that it also has proatherogenic effects within smooth vascular muscle as well [4].

== References ==

Sandbox Reserved 474: Difference between revisions

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@@ Line 35: / Line 35: @@
 == Mediator of Atherosclerosis ==
-It has been shown that at known concentrations, CRP elicits effects which result in either proinflammatory or proatherosclerotic phenotype [4].  Several in vitro experiments have shown CRP to downregulate eNOS transcription, thus destabilizing its mRNA, resulting in in a decreased release of basel and stimulated NO, key endothelial factors [4].  By inhibiting NO production, CRP effectively facilitates apoptosis and blocks angiogenesis.  Furthermore, it has been proposed that it is responsible for promoting the upregulation of nuclear factor-κB, which is a key promotor of several proatherosclerotic genes [4].  In addition, recent evidence has shown that it also has proatherogenic effects within smooth vascular muscle as well [1].
+It has been shown that at known concentrations, CRP elicits effects which result in either proinflammatory or proatherosclerotic phenotype [4].  Several in vitro experiments have shown CRP to downregulate eNOS transcription, thus destabilizing its mRNA, resulting in in a decreased release of basel and stimulated NO, key endothelial factors [4].  By inhibiting NO production, CRP effectively facilitates apoptosis and blocks angiogenesis.  Furthermore, it has been proposed that it is responsible for promoting the upregulation of nuclear factor-κB, which is a key promotor of several proatherosclerotic genes [4].  In addition, recent evidence has shown that it also has proatherogenic effects within smooth vascular muscle as well [4].
 == References ==