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Title: Activation of PKC{beta}{sub II} and PKC{theta} is essential for LDL-induced cell proliferation of human aortic smooth muscle cells via Gi-mediated Erk1/2 activation and Egr-1 upregulation

Journal Article · · Biochemical and Biophysical Research Communications
 [1]; ; ; ;  [1];  [2];  [3];  [4];  [5];  [1]
  1. Functional Genomics Research Center, Korea Research Institute of Bioscience and Biotechnology (KRIBB), Yuseong, Daejeon (Korea, Republic of)
  2. Bio-Evaluation Center, KRIBB, Yuseong, Daejeon (Korea, Republic of)
  3. Therapeutic Antibody Research Center, KRIBB, Yuseong, Daejeon (Korea, Republic of)
  4. Department of Pharmacy, Chungnam National University, Yuseong, Daejeon (Korea, Republic of)
  5. Department of Obstetrics and Gynecology, Inha University Hospital, Incheon (Korea, Republic of)

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 PKC{beta}{sub II} and PKC{theta} from cytosol to plasma membrane, and inhibition of PKC{beta}{sub II} and PKC{theta} decreased LDL effects via the deactivation of Erk1/2. Moreover, pertussis toxin, but not cholera toxin or heparin, inhibited LDL-induced translocation of PKC{beta}{sub II} and PKC{theta}, 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 PKC{beta}{sub II} and PKC{theta}. Inhibition of PKC{beta}{sub II} or PKC{theta}, 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 PKC{theta} in VSMC proliferation is unique.

OSTI ID:
21043674
Journal Information:
Biochemical and Biophysical Research Communications, Vol. 368, Issue 1; Other Information: DOI: 10.1016/j.bbrc.2008.01.050; PII: S0006-291X(08)00090-9; Copyright (c) 2008 Elsevier Science B.V., Amsterdam, The Netherlands, All rights reserved; Country of input: International Atomic Energy Agency (IAEA); ISSN 0006-291X
Country of Publication:
United States
Language:
English