Protein kinase C regulates vascular calcification via cytoskeleton reorganization and osteogenic signaling

Title
Protein kinase C regulates vascular calcification via cytoskeleton reorganization and osteogenic signaling
Author(s)
정대원이경희김현수
Keywords
SMOOTH-MUSCLE; ACTIN CYTOSKELETON; CELLS; HYPERPHOSPHATEMIA; DIFFERENTIATION; ACTIVATION; DISEASE; ALPHA
Issue Date
201410
Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
Citation
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, v.453, no.4, pp.793 - 797
Abstract
Vascular calcification is an active cell-mediated process that reduces elasticity of blood vessels and increases blood pressure. Until now, the molecular basis of vascular calcification has not been fully understood. We previously reported that microtubule disturbances mediate vascular calcification. Here, we found that protein kinase C (PKC) signaling acted as a novel coordinator between cytoskeletal changes and hyperphosphatemia-induced vascular calcification. Phosphorylation and expression of both PKC alpha and PKC delta decreased during inorganic phosphate (Pi)-induced vascular smooth muscle cell (VSMC) calcification. Knockdown of PKC isoforms by short interfering RNA as well as PKC inactivation by Go6976 or rottlerin treatment revealed that specific inhibition of PKC alpha. and PKC delta accelerated Pi-induced calcification both in VSMCs and ex vivo aorta culture through upregulation of osteogenic signaling. Additionally, inhibition of PKC alpha and PKC delta induced disassembly of microtubule and actin, respectively. In summary, our results indicate that cytoskeleton perturbation via PKC alpha, and PKC delta inactivation potentiates vascular calcification through osteogenic signal induction. (C) 2014 Elsevier Inc. All rights reserved.
URI
http://hdl.handle.net/YU.REPOSITORY/30665http://dx.doi.org/10.1016/j.bbrc.2014.10.026
ISSN
0006-291X
Appears in Collections:
의과대학 > 미생물학교실 > Articles
Files in This Item:
There are no files associated with this item.
Export
RIS (EndNote)
XLS (Excel)
XML


qrcode

Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.

BROWSE