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Ischaemic postconditioning protects isolated mouse hearts against ischaemia/reperfusion injury via sphingosine kinase isoform-1 activation.
| Content Provider | Semantic Scholar |
|---|---|
| Author | Jin, Zhu-Qiu Karliner, Joel S. Vessey, Donald A. |
| Copyright Year | 2008 |
| Abstract | AIMS Sphingosine-1-phosphate (S1P) plays a vital role in cytoskeletal rearrangement, development, and apoptosis. Sphingosine kinase-1 (SphK1), the key enzyme catalyzing the formation of S1P, mediates ischaemic preconditioning. Ischaemic postconditioning (POST) has been shown to protect hearts against ischaemia/reperfusion injury (IR). To date, no studies have examined the role of SphK1 in POST. METHODS AND RESULTS Wild-type (WT) and SphK1 null (KO) mouse hearts were subjected to IR (45 min of global ischaemia and 45 min of reperfusion) in a Langendorff apparatus. Left ventricular developed pressure (LVDP), maximum velocity of increase or decrease of LV pressure (+/-dP/dtmax), and LV end-diastolic pressure (LVEDP) were recorded. Infarction size was measured by 1% triphenyltetrazolium chloride staining. POST, consisting of 5 s of ischaemia and 5 s of reperfusion for three cycles after the index ischaemia, protected hearts against IR: recovery of LVDP and +/-dP/dtmax were elevated; LVEDP was decreased; infarction size (% of risk area) was reduced from 40 +/- 2% in the control group to 29 +/- 2% of the risk area in the POST group (P < 0.05, n = 4 per group). Phosphorylation of Akt and extracellular signal-regulated kinases detected by Western blotting was increased at 10 min of reperfusion. The protection induced by POST was abolished in KO hearts. Infarction size in KO hearts (57 +/- 5%) was not different from the KO control group (53 +/- 5% of risk area, n = 4, P = NS). CONCLUSIONS A short period of ischaemic POST protected WT mouse hearts against IR. The cardiac protection induced by POST was abrogated in SphK1-KO mouse hearts. Thus, SphK1 is critical for successful ischaemic POST. |
| File Format | PDF HTM / HTML |
| DOI | 10.1093/cvr/cvn065 |
| PubMed reference number | 18334546 |
| Journal | Medline |
| Volume Number | 79 |
| Issue Number | 1 |
| Alternate Webpage(s) | https://oup.silverchair-cdn.com/oup/backfile/Content_public/Journal/cardiovascres/79/1/10.1093/cvr/cvn065/2/cvn065.pdf?Expires=1493002014&Key-Pair-Id=APKAIUCZBIA4LVPAVW3Q&Signature=Wq8D9G0iYZ2bRhsIlbbhUD3j1pAWW9F7mKFkGQvPGCiornE3woBUTcn1Slysubw1-idXq3KszTBB7SYQRKwjSfMBQx3OsiS~1VUdO9IOky-sOjwuaDw9ma3sjwUhMfwKNgy9nxzhIX7I281a4Z6JguHwO4rBJUFYKjh96hb5KSIMJ-8jPIA6KAV2yRweTUAGR0mvVCd2gx-kVQPiHUY5VulN7XOmcZlLEcb4mtHs2~Gmp21I07xPlIJOmFAVXXw2cMqp4Thjw7zU8R6glKBbdak6SYWO8CuoiAJsaols5jGIfs-1QsnnX3C7Zse8ehbpdikl8zlUFV6JPmn8gjmZDA__ |
| Alternate Webpage(s) | https://doi.org/10.1093/cvr%2Fcvn065 |
| Journal | Cardiovascular research |
| Language | English |
| Access Restriction | Open |
| Content Type | Text |
| Resource Type | Article |
