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Dyslipidemia Induces Endothelial Cell Stiffening and Alterations in Angiogenic Potential
Author(s) -
Bogachkov Yedida,
Oh MyungJin,
Baruah Jugajyoti,
LeMaster Elizabeth,
Adamos Crystal,
Wary Kishore,
Levitan Irena
Publication year - 2015
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.29.1_supplement.956.5
Subject(s) - rhoa , stiffening , chemistry , angiogenesis , microbiology and biotechnology , dyslipidemia , medicine , cancer research , endocrinology , signal transduction , biology , biochemistry , materials science , composite material , obesity
Dyslipidemia is a modification in lipid composition that potentially causes adverse cardiovascular outcomes. An increase in oxidized low density lipoprotein (oxLDL), a common dyslipidemic condition, is considered to be detrimental. We show here that pathological levels of oxLDL induces endothelial cell (EC) stiffening and this stiffening is RhoA dependent. Furthermore, we tested the immediate downstream effector of RhoA, Rho kinase (ROCK). ROCK inhibition caused a complete abrogation of oxLDL induced EC stiffening. 7‐ketocholesterol (7KC), an important oxysterol component of oxLDL, has previously been shown to induce EC stiffening. We now extend our study to the inhibition of RhoA, which abolished the stiffening effect of 7KC. Previous studies have observed that oxLDL increases network formation in vitro. Here we now demonstrate that oxLDL increases migration and proliferation in vitro, and capillary formation in vivo. Similarly to oxLDL induced EC stiffening, the effects of oxLDL on angiogenesis were also inhibited by blocking RhoA and ROCK signaling. Additionally, PGPC and POVPC, components of oxLDL, were tested on capillary formation. We propose that oxLDL induced EC stiffening may play a potential role in angiogenesis under dyslipidemic conditions.