Remote ischaemic preconditioning involves signalling through the SDF-1α/CXCR4 signalling axis
| Autor: | Robert L. Yellon, Pradeep Selvaraj, David He, Claire Boi-Doku, Sean M. Davidson, Jose Miguel Vicencio, Derek M. Yellon |
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| Rok vydání: | 2013 |
| Předmět: |
Male
Chemokine Receptors CXCR4 Physiology Blotting Western Ischemia Enzyme-Linked Immunosorbent Assay Myocardial Reperfusion Injury Pharmacology CXCR4 Rats Sprague-Dawley hemic and lymphatic diseases Physiology (medical) medicine Animals Receptor Dipeptidyl peptidase-4 Cardioprotection biology business.industry medicine.disease Chemokine CXCL12 Rats Anesthesia Ischemic Preconditioning Myocardial biology.protein Stem cell Cardiology and Cardiovascular Medicine business Reperfusion injury Signal Transduction |
| Zdroj: | Basic research in cardiology. 108(5) |
| ISSN: | 1435-1803 |
| Popis: | Ischaemic preconditioning is one of the most potent experimental modalities known to decrease infarct size after ischaemia and reperfusion. Much interest has been stimulated by the phenomenon of remote ischaemic conditioning (RIC), in which the preconditioning stimulus is applied to a limb remote from the heart to stimulate cardioprotection via an unidentified humoral factor, believed to be a protein between 3.5 and 15 kDa. Stromal cell-derived factor-1 (SDF-1α or CXCL12) is a chemokine of 10 kDa that is induced by hypoxia and recruits stem cells, but also exerts direct, acute, cardioprotection via its receptor, CXCR4. The serum dipeptidase DPPIV cleaves and inactivates SDF-1α. We measured SDF-1α in rat plasma and found it was significantly increased by RIC. DPPIV activity was unchanged after RIC, suggesting that increased synthesis or release or SDF-1α caused the increase in plasma levels. AMD3100, a highly specific inhibitor of CXCR4, was used to investigate the hypothesis that SDF-1α is involved in RIC. RIC in rats, which decreased infarct size from 53 ± 3 % to 27 ± 3 % (n = 6, P |
| Databáze: | OpenAIRE |
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