Proteasome-dependent inactivation of Akt is essential for 12-O-tetradecanoylphorbol 13-acetate-induced apoptosis in vascular smooth muscle cells

被引：5

作者：

Fan, Yongna ^{[1
,2
]}

Xie, Ping ^{[1
,2
]}

Zhang, Hua ^{[1
,2
]}

Guo, Shubin ^{[3
]}

Gu, Dongfeng ^{[4
,5
,6
]}

She, Mingpeng ^{[1
,2
]}

Li, HuiHua ^{[1
,2
]}

机构：

[1] Tsinghua Univ, Chinese Acad Med Sci, Inst Basic Med Sci, Peking Union Med Coll,Dept Pathol, Beijing 100005, Peoples R China

[2] Tsinghua Univ, Chinese Acad Med Sci, Inst Basic Med Sci, Peking Union Med Coll,Natl Lab Med Mol Biol, Beijing 100005, Peoples R China

[3] Peking Union Med Hosp, Dept Acute Med, Beijing, Peoples R China

[4] Crdiovasc Inst, Div Populat Genet & Prevent, Beijing 100005, Peoples R China

[5] Chinese Acad Med Sci, Fuwai Hosp, Beijing 100005, Peoples R China

[6] Peking Union Med Coll, Beijing 100005, Peoples R China

来源：

APOPTOSIS | 2008年 / 13卷 / 12期

关键词：

Vascular smooth muscle cells; Apoptosis; 12-O-tetradecanoylphorbol; 13-acetate; Akt; Ubiquitin-proteasome system; PKC; PP2A;

D O I：

10.1007/s10495-008-0272-z

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Apoptosis of vascular smooth muscle cells (SMCs) is a prominent feature of blood vessel remodeling. Here we investigated the effect of 12-O-tetradecanoylphorbol 13-acetate (TPA) on SMC apoptosis. We found that TPA treatment induced SMC apoptosis through the rapid downregulation of Akt phosphorylation. The inhibition of Akt activation by TPA was markedly reduced by inhibitors of protein phosphatase 2A and proteasome. Moreover, TPA promoted the ubiquitination of p-Akt, whereas inhibition of TPA-induced PKC activation suppressed the downregulation and ubiquitination of p-Akt. Taken together, these results demonstrate that TPA triggers inactivation of Akt, at least in part, through PKC and Ubiquitin-proteasome degradation, thereby contributing to SMC apoptosis.

引用

页码：1401 / 1409

页数：9

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