January 1, 2007Endothelium

Cigarette Smoke-Induced Alterations in Endothelial Nitric Oxide Synthase Phosphorylation: Role of Protein Kinase C

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Population

Endothelial cell culture

Comparison

Cigarette smoke buffer treatment, followed by… vs Control (untreated) or CSB without inhibitors

Design

Preclinical

Authors

LWLászló WagnerSemmelweis University BLBoglárka LaczyUniversity of Würzburg MTMónika TamaskóUniversity of Würzburg

Discussion

Member takes

Implication

May link smoking to endothelial NO loss via PKC-eNOS in animals; leaves open human translation and therapeutic targeting.

Structured PICO

Population

Endothelial cell culture

Intervention

Cigarette smoke buffer (CSB) treatment, followed by reduced glutathione (GSH) or protein kinase inhibitors (H-89, LY-294002, Ro-318425, and ruboxistaurin)

Comparator

Control (untreated) or CSB without inhibitors

Outcome

eNOS phosphorylation at Ser(1177) and Thr(495), and eNOS dimer levelssurrogate

Cigarette smoke disrupts active eNOS dimers and shifts eNOS phosphorylation to an inhibitory state via a PKC-dependent mechanism, potentially explaining reduced NO bioavailability.

Cite This Study

Wagner et al. (2007) studied this question.

synapsesocial.com/papers/6a70ea81e71d69abee08ef9f https://doi.org/10.1080/10623320701606707

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Cigarette Smoke-Induced Alterations in Endothelial Nitric Oxide Synthase Phosphorylation: Role of Protein Kinase C

Discussion

Member takes

Implication

Structured PICO

Cite This Study

Cigarette Smoke-Induced Alterations in Endothelial Nitric Oxide Synthase Phosphorylation: Role of Protein Kinase C

Discussion

Member takes

Implication

Structured PICO

Cite This Study

Also Consider

Also Consider