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KMID : 0624620110440020140
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BMB Reports
2011 Volume.44 No. 2 p.140 ~ p.145
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PKC inhibitors RO 31-8220 and Go 6983 enhance epinephrine-induced platelet aggregation in catecholamine hypo-responsive platelets by enhancing Akt phosphorylation
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Kim Sun-Young
Kim Se-Woon
Kim Jeong-Mi
Jho Eek-Hoon
Park Seon-Yang
Oh Do-Yeun
Yun Hye-Sook
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Abstract
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Impaired responsiveness of platelets to epinephrine (epi) and other catecholamines (CA) has been reported in approximately 20% of the healthy Korean and Japanese populations. In the present study, platelet aggregation induced by epi was potentiated by RO 31-8220 (RO) or Go 6983 (Go). Phosphorylated Akt (p-Akt) was very low in epi-stimulated PRP from CA-hypo-responders (CA-HY), whereas it was detected in those from CA-good responders (CA-GR). RO and Go increased p-Akt, one of the major downstream effectors of phosphoinositol-3 kinase (PI3K), in epi-stimulated PRP from both groups. Wortmannin, a PI3K inhibitor, attenuated the RO or Go-induced potentiation of p-Akt in epi-stimulated PRP, suggesting positive effects for RO and Go on PI3K. TXA(2) formation was increased by the addition of either RO or Go in epi-stimulated platelets. The present data also suggest that impaired Akt phosphorylation may be responsible for epinephrine hypo-responsiveness of platelets.
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KEYWORD
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Akt, Epinephrine, Go 6983, Platelet aggregation, RO 31-8220
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