|本期目录/Table of Contents|

[1]范怡伦,吴佳伟,丁丹,等.Y编码样睾丸特异性蛋白5在心肌缺血再灌注损伤中的保护作用[J].国际心血管病杂志,2022,05:299-302.
　FAN Yilun,WU Jiawei,DING Dan,et al.The protective role of TSPYL5 in myocardial ischemia/reperfusion injury[J].International Journal of Cardiovascular Disease,2022,05:299-302.
点击复制

Y编码样睾丸特异性蛋白5在心肌缺血再灌注损伤中的保护作用(PDF)

《国际心血管病杂志》[ISSN:1006-6977/CN:61-1281/TN]

期数:
2022年05期
页码:
299-302
栏目:
基础研究
出版日期:
2022-10-01

文章信息/Info

Title:
The protective role of TSPYL5 in myocardial ischemia/reperfusion injury
作者:
范怡伦; 吴佳伟; 丁丹; 黄一航; 薛松; 黄日太
200127 上海交通大学医学院附属仁济医院心血管外科
Author(s):
FAN Yilun; WU Jiawei;  DING Dan;  HUANG Yihang;  XUE Song;  HUANG Ritai
Department of Cardiovascular Surgery, Renji Hospital, Shanghai Jiao Tong University School of Medicine, Shanghai 200127, China.
关键词:
Y 编码样睾丸特异性蛋白5 ; 心肌缺血再灌注损伤; 缺氧/ 复氧损伤; 凋亡; p53
Keywords:
TSPYL5;  Myocardial ischemia reperfusion injury;  Hypoxia/reoxygenation injury;  Cell apoptosis;  p53
分类号:
-
DOI:
10.3969/j.issn.1673-6583.2022.05.012
文献标识码:
-
摘要:
目的：观察过表达Y 编码样睾丸特异性蛋白5（TSPYL5）对缺氧/ 复氧损伤 后H9c2 细胞的影响。 方法：检测TSPYL5 在小鼠心肌缺血再灌注及心肌细胞缺氧/ 复氧 损伤后的表达水平。根据表达结果上调TSPYL5，以缺氧/ 复氧后普通H9c2 细胞为对照组， 相同模型中过表达TSPYL5 的H9c2 细胞为实验组，比较2 组间凋亡水平的差异。 结果： TSPYL5 在体内、体外实验中表达水平均显著下降（P＜0.001）。与对照组相比，缺氧/ 复 氧模型中过表达组p53 的蛋白表达水平显著下调（25.
Abstract:
Objective: To explore the effect of TSPYL5 overexpression on H9c2 cells after hypoxia/reoxygenation. Methods: We assessed the expression level of TSPYL5 after myocardial ischemia/reperfusion in mice and post hypoxia/reoxygenation in H9c2 cells, respective

参考文献/References

[1] Hausenloy DJ, Yellon DM. Targeting myocardial reperfusion injury—the search continues[J]. N Engl J Med, 2015, 373(11):1073-1075.
[2] Ib??ez, B, Heusch G, Qvize M, et al. Evolving therapies for myocardial ischemia/reperfusion injury[J]. J Am Coll Cardiol, 2015, 65(14):1454-1471.
[3] Ibá?ez B, Heusch G, Ovize M, et al. The protective role of curcumin in myocardial ischemia-reperfusion injury[J]. J Cell Physiol, 2018, 234(1):214-222.
[4] Fan Q, Tao R, Zhang H, et al. Dectin-1 contributes to myocardial ischemia/reperfusion injury by regulating macrophage polarization and neutrophil infiltration[J]. Circulation, 2019, 139(5):663-678.
[5] Hu G, Chong RA, Yang Q, et al. MTDH activation by 8q22 genomic gain promotes chemoresistance and metastasis of poor-prognosis breast cancer[J]. Cancer Cell, 2009, 15(1):9- 20.
[6] Epping MT, Meijer LA, Krijgsman O, et al. TSPYL5 suppresses p53 levels and function by physical interaction with USP7[J]. Nat Cell Biol, 2011, 13(1):102-108.
[7] Kim EJ, Lee SY, Kim TR, et al. TSPYL5 is involved in cell growth and the resistance to radiation in A549 cells via the regulation of p21(WAF1/Cip1) and PTEN/AKT pathway[J]. Biochem Biophys Res Commun, 2010, 392(3):448-453.
[8] Na HJ, Yeum CE, Kim HS, et al. TSPYL5-mediated inhibition of p53 promotes human endothelial cell function[J]. Angiogenesis, 2019, 22(2):281-293.
[9] Vaseva AV, Moll UM. The mitochondrial p53 pathway[J]. Biochim Biophys Acta, 2009, 1787(5):414-420.
[10] Vousden KH, Lane DP. p53 in health and disease[J]. Nat Rev Mol Cell Biol, 2007, 8(4):275-283.
[11] Ma S, Sun L, Wu W, et al. USP22 protects against myocardial ischemia-reperfusion injury via the SIRT1-p53/SLC7A11- dependent inhibition of ferroptosis-induced cardiomyocyte death[J]. Front Physiol, 2020, 11:551318.
[12] Zhang H, Wang J, Du A, et al. MiR-483-3p inhibition ameliorates myocardial ischemia/reperfusion injury by targeting the MDM4/p53 pathway[J]. Mol Immunol, 2020, 125:9-14.

备注/Memo

备注/Memo:
基金项目：上海交大医学院附属仁济医院临床科研创新培育基金计 划（PYMDT-008）
通信作者：黄日太， E-mail：huangritai@renji.com
更新日期/Last Update: 2022-10-01