July 13, 1998Circulation Research
Genetic Disruption of Poly (ADP-Ribose) Synthetase Inhibits the Expression of P-Selectin and Intercellular Adhesion Molecule-1 in Myocardial Ischemia/Reperfusion Injury
Key result
Genetic disruption or pharmacological inhibition of PARS reduced the expression of P-selectin and ICAM-1, protecting against myocardial ischemia and reperfusion injury.
Why the study?
Does genetic disruption or pharmacological inhibition of PARS reduce myocardial ischemia/reperfusion injury by inhibiting P-selectin and ICAM-1 expression?
Population
Preclinical models including animals with genetic disruption of PARS, fibroblasts lacking functional PARS…
Comparison
Genetic disruption of PARS or pharmacological… vs Animals with normal genotype or untreated cells
Design
Preclinical
Authors
Discussion
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Implication
PARS emerges as a target to limit ischemia-reperfusion injury; leaves open whether inhibition improves clinical outcomes.
Structured PICO
Does genetic disruption or pharmacological inhibition of PARS reduce myocardial ischemia/reperfusion injury by inhibiting P-selectin and ICAM-1 expression?
P
Population
Preclinical models including animals with genetic disruption of PARS, fibroblasts lacking functional PARS gene, and cultured human endothelial cells
I
Intervention
Genetic disruption of PARS or pharmacological inhibition of PARS by 3-aminobenzamide
C
Comparator
Animals with normal genotype or untreated cells
O
Outcome
Expression of P-selectin and intercellular adhesion molecule-1 (ICAM-1) and recruitment of neutrophils into jeopardized tissuesurrogate
Inhibition of PARS protects against myocardial ischemia/reperfusion injury by reducing P-selectin and ICAM-1 expression and subsequent neutrophil recruitment, suggesting a novel therapeutic target.
Cite This Study
Zingarelli et al. (1998) studied Myocardial ischemia/reperfusion injury. Genetic disruption or pharmacological inhibition of PARS vs. Normal genotype or no inhibition was evaluated on Expression of P-selectin and ICAM-1 and recruitment of neutrophils. Genetic disruption or pharmacological inhibition of PARS reduced the expression of P-selectin and ICAM-1, protecting against myocardial ischemia and reperfusion injury.