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

Cited 16 time in scopus
Metadata Downloads
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
Author(s)
Kyung Sun Heo; Dong Uk Kim; L Kim; Miyoung Nam; Seung-Tae Baek; Song Kyu Park; Young Woo Park; C S Myung; S O Hwang; Kwang Lae Hoe
Bibliographic Citation
Biochemical and Biophysical Research Communications, vol. 368, no. 1, pp. 126-131
Publication Year
2008
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.
Keyword
Egr-1Erk1/2 MAPKGPCRLow-density lipoproteinPKCSmooth muscle cell
ISSN
0006-291X
Publisher
Elsevier
DOI
http://dx.doi.org/10.1016/j.bbrc.2008.01.050
Type
Article
Appears in Collections:
Division of Biomedical Research > Rare Disease Research Center > 1. Journal Articles
Files in This Item:
  • There are no files associated with this item.


Items in OpenAccess@KRIBB are protected by copyright, with all rights reserved, unless otherwise indicated.