Protection of endothelial cells against Ang II-induced impairment: Involvement of both PPAR and PPAR via PI3K/Akt pathway

被引：7
作者：
Shan, HaiYan [1 ]
Zhang, Siyang [2 ]
Wei, Xiaojie [1 ]
Li, Xuelian [3 ]
Qi, Huimeng [1 ]
He, Yini [1 ]
Liu, Ao [1 ]
Luo, Donghui [1 ]
Yu, Xiaosong [1 ]
机构：
[1] China Med Univ, Dept Gen Practice, Affiliated Hosp 1, 155 Nanjing North St, Shenyang 110001, Liaoning Provin, Peoples R China
[2] China Med Univ, Sci Expt Ctr, Shenyang, Peoples R China
[3] China Med Univ, Dept Epidemiol, Coll Publ Hlth, Shenyang, Peoples R China
来源：
CLINICAL AND EXPERIMENTAL HYPERTENSION | 2016年 / 38卷 / 07期
基金：
中国国家自然科学基金;
关键词：
Angiotensin II; endothelial dysfunction; PI3K; Akt pathway; PPAR; ACTIVATED RECEPTOR-GAMMA; ANGIOTENSIN-II; TYPE-1; RECEPTOR; APOPTOSIS; RATS; DYSFUNCTION; INJURY; HYPERTENSION; AKT;
D O I：
10.3109/10641963.2016.1174248
中图分类号：
R9 [药学];
学科分类号：
1007 ;
摘要：
The aim of our study is to explore the involvement of PPAR and PPAR in Ang II-induced endothelial injury. We found that Ang II significantly elevated the oxidative stress in HUVECs, causing apoptosis and cellular impairment in a time-dependent pattern. Activation of either PPAR by docosahexaenoic acid (DHA) or PPAR by rosiglitazone protected the endothelial cells. Interestingly, a more significant effect was observed when DHA and rosiglitazone were administrated together. Moreover, we found that this protection was mediated through the PI3K/Akt pathway. Our study may help to understand the mechanism of endothelial dysfunction, contributing to the treatment of hypertension and other endothelial-related diseases.
引用
收藏
页码：571 / 577
页数：7
相关论文
共 22 条
  • [1] Endothelial cell apoptosis induced by the peroxisome proliferator-activated receptor (PPAR) ligand 15-deoxy-Δ12,14-prostaglandin J2
    Bishop-Bailey, D
    Hla, T
    [J]. JOURNAL OF BIOLOGICAL CHEMISTRY, 1999, 274 (24) : 17042 - 17048
  • [2] Chinetti G, 2001, Z Kardiol, V90 Suppl 3, P125
  • [3] Role of endothelial dysfunction in atherosclerosis
    Davignon, J
    Ganz, P
    [J]. CIRCULATION, 2004, 109 (23) : 27 - 32
  • [4] PPARα activator effects on Ang II-induced vascular oxidative stress and inflammation
    Diep, QN
    Amiri, F
    Touyz, RM
    Cohn, JS
    Endemann, D
    Neves, MF
    Schiffrin, EL
    [J]. HYPERTENSION, 2002, 40 (06) : 866 - 871
  • [5] PPAR activators inhibit endothelial cell migration by targeting Akt
    Goetze, S
    Eilers, F
    Bungenstock, A
    Kintscher, U
    Stawowy, P
    Blaschke, F
    Graf, K
    Law, RE
    Fleck, E
    Gräfe, M
    [J]. BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 2002, 293 (05) : 1431 - 1437
  • [6] Soluble epoxide hydrolase inhibition and peroxisome proliferator activated receptor γ agonist improve vascular function and decrease renal injury in hypertensive obese rats
    Imig, John D.
    Walsh, Katie A.
    Khan, Md Abdul Hye
    Nagasawa, Tasuku
    Cherian-Shaw, Mary
    Shaw, Sean M.
    Hammock, Bruce D.
    [J]. EXPERIMENTAL BIOLOGY AND MEDICINE, 2012, 237 (12) : 1402 - 1412
  • [7] Inoue Ikuo, 2003, J Atheroscler Thromb, V10, P99
  • [8] Evaluation of PPARγ agonists on rodent endothelial cell proliferation
    Kakiuchi-Kiyota, Satoko
    Arnold, Lora L.
    Yokohira, Masanao
    Suzuki, Shugo
    Pennington, Karen L.
    Cohen, Samuel M.
    [J]. TOXICOLOGY, 2011, 287 (1-3) : 91 - 98
  • [9] The PPAR-γ agonist rosiglitazone facilitates Akt rephosphorylation and inhibits apoptosis in cardiomyocytes during hypoxia/reoxygenation
    Kilter, H.
    Werner, M.
    Roggia, C.
    Reil, J. -C.
    Schaefers, H.-J.
    Kintscher, U.
    Boehm, M.
    [J]. DIABETES OBESITY & METABOLISM, 2009, 11 (11) : 1060 - 1067
  • [10] Biphasic effects of 15-deoxy-Δ12,14-prostaglandin J2 on glutathione induction and apoptosis in human endothelial cells
    Levonen, AL
    Dickinson, DA
    Moellering, DR
    Mulcahy, RT
    Forman, HJ
    Darley-Usmar, VM
    [J]. ARTERIOSCLEROSIS THROMBOSIS AND VASCULAR BIOLOGY, 2001, 21 (11) : 1846 - 1851
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