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A more recent version of this article appeared on December 1, 2003

Papers In Press, published online ahead of print September 1, 2003
J. Lipid Res., doi:10.1194/jlr.M300266-JLR200
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Submitted on June 18, 2003
Revised on August 19, 2003
Accepted on August 19, 2003

LDLs induce fibroblast spreading independently of the LDL receptor via activation of the p38 MAPK pathway

Iveta Dobreva, Gérard Waeber, Vincent Mooser, Richard W. James, and Christian Widmann

Institute of Cellular Biology and Morphology (IBCM), Lausanne 1005

Corresponding Author: Christian.Widmann{at}ibcm.unil.ch

Since adventitial fibroblasts play an important role in the repair of blood vessels, we assessed whether elevation in LDL concentrations would affect fibroblast function and whether this depended on activation of intracellular signaling pathways. We show here that in primary human fibroblasts, LDLs induced transient activation of the p38 mitogen-activated protein kinase (MAPK) pathway, but not the c-Jun N-terminal kinase (JNK) MAPK pathway. This activation did not require the recruitment of the LDL receptor (LDLR) because LDLs efficiently stimulated the p38 MAPK pathway in human and mouse fibroblasts lacking functional LDLR and since receptor-associated protein (RAP), an LDLR family antagonist, did not block the LDL-induced p38 activation. LDL particles also induced lamellipodia formation and cell spreading. These effects were blocked by SB203580, a specific p38 inhibitor. Our data demonstrate that LDLs can regulate the shape of fibroblasts in a p38 MAPK-dependent manner, a mechanism that may participate in wound healing or during vessel remodeling as in atherosclerosis.


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I. Dobreva, G. Waeber, R. W. James, and C. Widmann
Interleukin-8 Secretion by Fibroblasts Induced by Low Density Lipoproteins Is p38 MAPK-dependent and Leads to Cell Spreading and Wound Closure
J. Biol. Chem., January 6, 2006; 281(1): 199 - 205.
[Abstract] [Full Text] [PDF]


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