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Ischemic preconditioning-induced cardioprotection is lost in mice with immunoproteasome subunit low molecular mass polypeptide-2 deficiency
Cai, Zheqing P.1; Shen, Zhenyun2; Van Kaer, Luc; Becker, Lewis C.1
关键词ubiquitin-proteasome system reperfusion injury ubiquitin phosphatase and tensin homologue deleted on chromosome 10 PTEN Akt
刊名FASEB JOURNAL
2008-12-01
DOI10.1096/fj.08-105940
22期:12页:4248-4257
收录类别SCI
文章类型Article
WOS标题词Science & Technology
类目[WOS]Biochemistry & Molecular Biology ; Biology ; Cell Biology
研究领域[WOS]Biochemistry & Molecular Biology ; Life Sciences & Biomedicine - Other Topics ; Cell Biology
关键词[WOS]PROTEIN-KINASE-C ; UBIQUITIN-PROTEASOME SYSTEM ; TUMOR-SUPPRESSOR PTEN ; VENTRICULAR HYPERTROPHY ; DAMAGED PROTEINS ; 26S PROTEASOME ; UP-REGULATION ; LMP2 ; DEGRADATION ; MYOCARDIUM
英文摘要

The ubiquitin-proteasome system plays an important role in many cellular processes through degradation of specific proteins. Low molecular mass polypeptide 2 (LMP-2 or beta(1i)) is one important subunit of the immunoproteasome. Ischemic preconditioning (IPC) activates cell signaling pathways and generates cardioprotection but has not been linked to LMP-2 function previously. LMP-2 knockout mice (C57BL6 background) and wild-type C57BL6 mice were subjected to 30 min of ischemia (I-30) and 120 min of reperfusion (R-120) with or without preceding IPC (10 min of infusion and 5 min of reperfusion). IPC significantly increased left ventricular developed pressure and decreased infarct size in wild-type mice, but this protective effect of IPC was lost in LMP-2 knockout mice. IPC-mediated degradation of phosphatase and tensin homologue deleted on chromosome 10 (PTEN) and activation of the downstream protein kinase Akt were impaired in LMP-2 knockout hearts. The impairment of PTEN degradation was associated with defective immunoproteasomes and decreased proteolytic activities. When LMP-2 knockout mice were pretreated with the PTEN inhibitor bpV(HOpic), cardiac function was significantly improved, and myocardial infarct size was significantly reduced after I-30/R-120. In conclusion, LMP-2 is required for normal proteasomal function and IPC induction in the heart. Its action may be related to PTEN protein degradation.

语种英语
WOS记录号WOS:000261254800024
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被引频次:39[WOS]   [WOS记录]     [WOS相关记录]
文献类型期刊论文
条目标识符http://ir.bjmu.edu.cn/handle/400002259/58411
专题北京大学第三临床医学院_胸外科
作者单位1.Johns Hopkins Univ, Sch Med, Dept Med, Div Cardiol, Baltimore, MD 21205 USA
2.Peking Univ, Hosp 3, Dept Thorac Surg, Beijing 100871, Peoples R China
3.Vanderbilt Univ, Sch Med, Dept Microbiol & Immunol, Nashville, TN 37212 USA
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GB/T 7714
Cai, Zheqing P.,Shen, Zhenyun,Van Kaer, Luc,et al. Ischemic preconditioning-induced cardioprotection is lost in mice with immunoproteasome subunit low molecular mass polypeptide-2 deficiency[J]. FASEB JOURNAL,2008,22(12):4248-4257.
APA Cai, Zheqing P.,Shen, Zhenyun,Van Kaer, Luc,&Becker, Lewis C..(2008).Ischemic preconditioning-induced cardioprotection is lost in mice with immunoproteasome subunit low molecular mass polypeptide-2 deficiency.FASEB JOURNAL,22(12),4248-4257.
MLA Cai, Zheqing P.,et al."Ischemic preconditioning-induced cardioprotection is lost in mice with immunoproteasome subunit low molecular mass polypeptide-2 deficiency".FASEB JOURNAL 22.12(2008):4248-4257.
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