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Title 

Activation of PKCβII and PKCθ is essential for LDL-induced cell proliferation of human aortic smooth muscle cells via Gi-mediated Erk1/2 activation and Egr-1 upregulation

Authors 

Kyung Sun HeoDong Uk KimL KimMiyoung NamSeung-Tae BaekSong Kyu ParkYoung Woo ParkC S MyungS O HwangKwang Lae Hoe

Publisher 

Elsevier

Issue Date 

2008

Citation 

Biochemical and Biophysical Research Communications, vol. 368, no. 1, pp. 126-131

Keywords 

Egr-1Erk1/2 MAPKGPCRlow-density lipoproteinPKCsmooth muscle cellearly growth response factor 1mitogen activated protein kinase 1protein kinase C beta iicell proliferation

Abstract 

Native LDL may be a mitogenic stimulus of VSMC proliferation in lesions where endothelial disruption occurs. Recent studies have demonstrated that the mitogenic effects of LDL are accompanied by Erk1/2 activation via an unknown G-protein-coupled receptor (GPCR). In this article, we report that LDL translocated PKCβII and PKCθ from cytosol to plasma membrane, and inhibition of PKCβII and PKCθ decreased LDL effects via the deactivation of Erk1/2. Moreover, pertussis toxin, but not cholera toxin or heparin, inhibited LDL-induced translocation of PKCβII and PKCθ, suggesting that Gi protein plays a role in LDL effects. of LPA, S1P, and LDL, whose signaling is conveyed via Gi/o proteins, only LDL induced translocation of PKCβII and PKCθ. Inhibition of PKCβII or PKCθ, as well as of Erk1/2 and GPCR, decreases LDL-induced upregulation of Egr-1, which is critical for cell proliferation. This is the first report, to our knowledge, that the participation of PKCθ in VSMC proliferation is unique.

ISSN 

0006-291X

Link 

http://dx.doi.org/10.1016/j.bbrc.2008.01.050

Appears in Collections

1. Journal Articles > Journal Articles

Registered Date

2019-05-02


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