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| Content Provider | PubMed Central |
|---|---|
| Author | Vessey, Donald A. Li, Luyi Jin, Zhu-qiu Kelley, Michael Norman, Honbo Zhang, Jianqing Karliner, Joel S. |
| Copyright Year | 2011 |
| Abstract | Sphingosine kinase (SphK) exhibits two isoforms, SphK1 and SphK2. Both forms catalyze the synthesis of sphingosine 1-phosphate (S1P), a sphingolipid involved in ischemicpreconditioning (IPC). Since the ratio of SphK1 : SphK2 changes dramatically with aging, it is important to assess the role of SphK2 in IR injury and IPC. Langendorff mouse hearts were subjected to IR (30 minequilibration, 50 min global ischemia, and 40 min reperfusion). IPC consisted of 2 min of ischemia and 2 min of reperfusion for two cycles. At baseline, there were no differences in left ventricular developed pressure (LVDP), ± dP/dtmax, and heart rate between SphK2 null (KO)and wild-type (WT) hearts. In KO hearts, SphK2 activity was undetectable, and SphK1 activity was unchanged compared to WT. Total SphK activity was reduced by 53%. SphK2 KO hearts subjected to IR exhibited significantly more cardiac damage (37 ± 1%infarct size) compared with WT (28 ± 1% infarct size); postischemic recovery of LVDPwas lower in KO hearts. IPC exerted cardioprotection in WT hearts. The protectiveeffect of IPC against IR was diminished in KO hearts which had much higher infarction sizes (35 ± 2%) compared to the IPC/IR group in control hearts (12 ± 1%). Western analysis revealed that KOhearts had substantial levels of phosphorylated p38 which could predispose theheart to IR injury. Thus, deletion of the SphK2 gene sensitizes the myocardium to IR injury anddiminishes the protective effect of IPC. |
| Related Links | http://dx.doi.org/10.1155/2011/961059 |
| Starting Page | 961059 |
| File Format | |
| ISSN | 19420900 |
| e-ISSN | 19420994 |
| Journal | Oxidative Medicine and Cellular Longevity |
| Volume Number | 2011 |
| Language | English |
| Publisher | Hindawi Publishing Corporation |
| Publisher Date | 2011-01-01 |
| Access Restriction | Open |
| Rights Holder | Hindawi Publishing Corporation |
| Subject Keyword | Cell Biology Biochemistry Ageing Research in Higher Education |
| Content Type | Text |
| Resource Type | Article |
| Subject | Cell Biology Aging Medicine Biochemistry |
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