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Sachinidis et al., Arterioscler Thromb Vasc Biol 1999 : LDL , HDL, and VLDL stimulate ERK1/2 with the following order of potency : LDL > HDL > VLDL
Jenkins et al., Diabetes 2000 : Therefore, we examined the effects of LDL on ERK phosphorylation in cultured rat mesangial cells
Velarde et al., J Appl Physiol 2001 (Arteriosclerosis...) : Therefore, we examined the cellular effects of native and modified LDL on ERK phosphorylation in VSMC ... Treatment of VSMC with the intracellular Ca ( 2+ ) chelator EGTA-AM ( 50 micromol/l ) significantly increased ERK phosphorylation induced by native and mildly modified LDL, whereas chelation of extracellular Ca ( 2+ ) by EGTA ( 3 mmol/l ) significantly reduced LDL induced ERK phosphorylation ... Downregulation of PKC with phorbol myristate acetate ( 5 micromol/l ) markedly reduced LDL induced ERK phosphorylation ... Pretreatment of VSMC with a cell-permeable MEK inhibitor ( PD-98059, 40 micromol/l ) significantly decreased ERK phosphorylation in response to native and modified LDL
Cai et al., Circulation 2004 (Cardiovascular Diseases...) : When added to human endothelial cells ( ECV 304 or human umbilical vein endothelial cells ), Db-HAGE-LDL promoted marked ERK1/2 phosphorylation ( pERK1/2) (5.5- to 10-fold of control ) in a time- and dose dependent manner compared with Db-LAGE-LDL or native LDL
Cho et al., Mol Cells 2005 (MAP Kinase Signaling System) : ERK phosphorylation was not affected by exposure to the Ca2+ chelator BAPTA-AM but inhibition of protein kinase C ( PKC ) with GF109203X, inhibition of Src kinase with PP1 ( 5 microM ) and inhibition of phospholipase C (PLC) with U73122/U73343 ( 5 microM ) all reduced ERK phosphorylation in response to glycated LDL ... In addition, pretreatment of the RASMCs with a cell-permeable mitogen activated protein kinase kinase ( MEK ) inhibitor ( PD98059, 5 microM ) markedly decreased ERK phosphorylation in response to native and glycated LDL ... These findings indicate that ERK phosphorylation in response to glycated LDL involves the activation of PKC, PLC, and MEK, but is independent of intracellular Ca2+
Anwar et al., Free Radic Biol Med 2005 (Arteriosclerosis...) : These findings demonstrate for the first time that activation of PKC, p38 ( MAPK ), JNK, ERK1/2 , and Nrf2 by oxidized LDL in human SMC leads to HO-1 induction, constituting an adaptive response against oxidative injury that can be ameliorated by vitamin C
Tanigawa et al., Atherosclerosis 2006 : In addition, both minimally and extensively Ox-LDL induced similar levels of ERK1/2 activation through Lox-1 in human coronary artery smooth muscle cells
Hong et al., Translational research : the journal of laboratory and clinical medicine 2006 : This study examines whether an interaction exists between Ox-LDL induced TGF-beta/Smad signaling pathways and ERK activation leading to PAI-1 transcription in human mesangial cells ... Ox-LDL ( 50 microg/mL ) induced an acute increase in ERK activity within 15 min, which decreased to control value at 2 h. Incubation with anti-TGF-beta or SB-431542, an inhibitor of the TGF-beta type I receptor, along with Ox-LDL, inhibited the expected increase in ERK phosphorylation ... These results suggest that phosphorylation of ERK is induced by Ox-LDL through the induction of the TGF-beta signaling pathway and that activated ERK, in turn, participates in the Ox-LDL induced Smad3 activation and subsequent PAI-1 gene expression in mesangial cells
Song et al., Translational research : the journal of laboratory and clinical medicine 2008 (MAP Kinase Signaling System) : Quiescent mesangial cells were incubated for 18 h with and without the presence of lovastatin before 50 microg/mL of Ox-LDL treatment for 1 h. Lovastatin inhibited markedly the stimulatory effects of Ox-LDL on ERK1/2 activation, nuclear Smad3 expression, TGF-beta1 and PAI-1 mRNA and protein expression, and PAI-1 luciferase activity ... Similar to lovastatin, FTI-277, which is an inhibitor of Ras farnesylation, decreased the Ox-LDL induced activation of ERK/Smad3 and induction of TGF-beta1/PAI-1 ... These results indicate that lovastatin prevents the Ox-LDL induced Ras/ERK activation that results in inhibition of Smad3 activation in mesangial cells with subsequent downregulation of TGF-beta target genes
Taketa et al., J Biol Chem 2008 (Atherosclerosis...) : Ox-LDL induced phosphorylation of ERK1/2 and p38 MAPK, and ERK1/2 specific inhibition abrogated Ox-LDL induced COX-2 expression and PPARalpha and PPARgamma activation, whereas p38 MAPK-specific inhibition had no effect
Sangle et al., Am J Physiol Endocrinol Metab 2008 : Treatment with PD-98059, an ERK1/2 inhibitor, blocked C-oLDL or LDL induced ERK1/2 phosphorylation or PAI-1 expression in EC
Béaslas et al., PloS one 2009 : These early events included the trafficking of apolipoprotein B , a structural component of TRL, from apical towards secretory domains, and the rapid, dose dependent activation of ERK and p38MAPK
Ishii et al., J Biol Chem 2009 : AICAR partially suppressed Ox-LDL induced ERK1/2 phosphorylation and GM-CSF expression, suggesting that another mechanism is also involved in the AICAR mediated suppression of macrophage proliferation
Li et al., Chin J Integr Med 2012 (Atherosclerosis...) : The expression of phospho-ERK1/2 was increased in the presence of ox-LDL compared with the control cells ( P < 0.01 ), but no significant differences existed between the cells cultured in the presence of ox-LDL+andrographolide and the control medium ( P > 0.05 ) ... Andrographolide could inhibit the activation of ERK1/2 , p38MAPK and NK-?B induced by ox-LDL in macrophage foam cells, which might be one of its mechanisms in preventing atherosclerosis
El-Shewy et al., Mol Endocrinol 2012 (Diabetic Nephropathies...) : In these cells, treatment with pertussis toxin abolished LDL stimulated activation of ERK1/2 and c-Jun N-terminal kinase (JNK), indicating the involvement of heterotrimeric G proteins in LDL signaling ... Pretreating cells with SK inhibitor, dimethylsphinogsine or down-regulation of SK1 and SK2 revealed that LDL dependent activation of ERK1/2 and JNK is mediated by SK1
Wang et al., Cardiovasc Drugs Ther 2013 (Atherosclerosis...) : Furthermore, TMP suppressed ox-LDL induced activations of p-ERK , p-p38, and p-JNK MAPK