Reperfusion kinase phosphorylation is essential but not sufficient in the mediation of pharmacological preconditioning: Characterisation in the bi-phasic profile of early and late protection | Zendy

Rachel E. Bell | Zendy; James Clark | Zendy; David J. Hearse | Zendy; Michael J. Shattock | Zendy

Open Access

Reperfusion kinase phosphorylation is essential but not sufficient in the mediation of pharmacological preconditioning: Characterisation in the bi-phasic profile of early and late protection

Author(s) -

Rachel E. Bell,

James Clark,

David J. Hearse,

Michael J. Shattock

Publication year - 2006

Publication title -

cardiovascular research

Language(s) - English

Resource type - Journals

SCImago Journal Rank - 2.774

H-Index - 219

eISSN - 1755-3245

pISSN - 0008-6363

DOI - 10.1016/j.cardiores.2006.10.013

Subject(s) - wortmannin , kinase , protein kinase b , mapk/erk pathway , phosphorylation , angiotensin ii , ischemic preconditioning , pharmacology , medicine , chemistry , microbiology and biotechnology , ischemia , endocrinology , biology , receptor

Pharmacological preconditioning (PPC) triggers early (ePPC) and delayed protection (dPPC), occurring within 1 h or after 24 h following the preconditioning stimulus, respectively, through recruitment of protein kinase signalling. Angiotensin II (ATII) is a recognised trigger of PPC, recruiting kinases and transcription factors known to be involved in both phases of protection. Our objectives were to determine whether ATII is capable of triggering dPPC and whether recruitment of pro-survival kinases, Akt and extracellular signal-regulated kinase (ERK), following the injurious ischaemic insult is essential for the mediation of PPC.

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