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Rabini et al., J Clin Endocrinol Metab 1999 (Diabetes Mellitus, Type 1) : IDDM LDL significantly increased the platelet aggregating response to ADP, cytosolic Ca2+ concentrations, and plasma membrane Ca2+-ATPase activity and significantly reduced NOS activity and platelet membrane Na+/K+-ATPase activity compared with those of platelets incubated in buffer or cells incubated with control LDL
Zabe et al., Cell Calcium 1999 : We have previously demonstrated that Cu ( 2+ ) -oxidized LDL inhibits platelet plasma membrane Ca ( 2+ ) -ATPase ( PMCA ) in isolated membranes and causes an increase in cytosolic Ca2+ in resting whole platelets ... Since platelet function may be affected by native and modified lipoproteins, the effect of HOCl modified LDL and HDL3 on platelet PMCA and on the free intracellular Ca2+ concentration ([Ca2+]i) of whole platelets has been investigated
Bochkov et al., Atherosclerosis 1992 (Hyperlipoproteinemia Type II) : We have found that in accordance with previous results LDL induced instant reversible elevation of free cytoplasmic calcium concentration ( [ Ca2+ ] i ) in fura-2 loaded platelets
He et al., Life Sci 2005 (Arteriosclerosis) : In the presence or absence of extracellular Ca2+ , crocin concentration-dependently inhibited the [ Ca2+ ] i elevation induced by 120 mg x L ( -1 ) Ox-LDL , In the absence of extracellular Ca2+, crocin could inhibit the [ Ca2+ ] i elevation induced by CHCl3 in a concentration dependent manner
Zuliani et al., Platelets 1998 : The present study tested the effects of ox-low density lipoprotein (LDL) on nitric oxide ( NO ) -dependent decrease in agonist stimulated [Ca2+ ] i ... Ox-LDL did not cause any increase in thrombin induced [Ca2+ ] ( control : 215.4 +/- 44.3 nmol/l, ox-LDL 223.4 +/- 35.3 nmol/l, M +/- SEM ; n = 8 ) and platelet aggregation ( control : 78.7 +/- 4.9 %, ox-LDL : 78.9 +/- 4.2 %, n = 12 )
Seres et al., Cell Biochem Funct 2007 (Calcium Signaling) : LDL in 10 microg ml(-1) concentration could induce inositol trisphosphate ( IP3 ) and Ca2+ signal generation through a pertussis toxin ( PT ) sensitive G protein in human monocytes
Srinivasan et al., Biochim Biophys Acta 1991 : Although both heparin preparations formed insoluble complexes with LDL quantitatively in the presence of 30 mM Ca2+ , the concentrations of NaCl required for 50 % reduction in maximal insoluble complex formation was markedly higher with high-affinity subfraction ( 0.55 M vs. 0.04 M )
Bochkov et al., Thromb Res 1991 (Coronary Disease...) : LDL induced a reversible increase in [Ca2+ ] i in platelets of healthy subjects and FH-patients
Galle et al., Eicosanoids 1990 : LDL oxidized by incubation with Cu2+ had no immediate effects on [Ca2+ ] i when applied at a concentration of 80 micrograms/ml, whereas 160 micrograms/ml, in the presence of 1 mmol/l extracellular Ca2+, elicited increases in [ Ca2+ ] i and PGI2 release
Gherardi et al., Biochem J 1988 : The purified receptor exhibited all the properties of the membrane bound receptor including Ca2+ dependent binding of rabbit and human LDL but not of methylated LDL or high density lipoprotein
Wegrowski et al., Biochem J 1986 : PGI and PGII formed insoluble complexes with human LDL in the presence of Ca2+
Kecskés et al., Thromb Haemost 1983 : Heparin forms a complex with human low density lipoprotein (LDL) in the presence of Ca2+
Mazurov et al., Biokhimiia 1982 : The binding of LDL to platelets is reversible and independent of Ca2+
Mourão et al., Atherosclerosis 1984 : Aortic and cartilaginous glycosaminoglycans are retained in LDL affinity columns and produce turbidity when added to LDL in presence of Ca2+
Zhao et al., Thromb Res 1993 : LDL promoted the increase of [Ca2+ ] i ( 471 +/- 31 nM ) induced by thrombin ( 0.03 U/ml ) as compared to that which thrombin did alone ( 240 +/- 11 nM ) ( p < 0.05 )
Standley et al., Am J Hypertens 1993 (Diabetes Mellitus, Type 2...) : To determine the possible role of hyperinsulinemia in this accentuated [ Ca2+ ] i response to LDL, we measured basal and LDL stimulated [ Ca2+ ] i in platelets of normal volunteers after insulin treatment ( 0-100 mU/mL for 30 and 90 min )
Liu et al., J Biol Chem 1993 : Lowering the extracellular Ca2+ concentration removed the stimulatory effect of LDL on the Ca2+ transient
Möllers et al., Cell Signal 1995 (Second Messenger Systems) : In fura-2 loaded suspended fibroblasts, HDL3 and LDL increased intracellular Ca2+ concentrations ([Ca2+]i) with comparable rapid, transient kinetics ... The dose-profiles for HDL3- and LDL induced increases in [ Ca2+ ] i were also comparable, with half-maximally and maximally effective concentrations being approximately 15 micrograms/mL and approximately 50 micrograms/mL, respectively
Wells et al., Surgery 1996 (Second Messenger Systems) : Oxidized LDL induced Ca+2-cAMP signaling modulates the cellular oxidation of N-LDL
Sachinidis et al., Mol Pharmacol 1997 : Stimulation of VSMCs with LDL resulted in a pertussis-toxin ( PTX ) -sensitive stimulation of the 44-kDa mitogen activated protein ( MAP ) kinase ( p44(mapk) ) and 42-kDa MAP kinase ( p42(mapk) ) isoforms as well as in a PTX-sensitive increase in intracellular free Ca2+ concentration ([Ca2+]i) ... In contrast, the LDL induced increase in [ Ca2+ ] i may be implicated in this process only in conjugation with other signaling components
Skinner et al., J Hypertens 1998 (Arteriosclerosis...) : Ca2+ plays an important role in biochemical processes involved in blood pressure regulation and can be activated by low-density lipoprotein (LDL) cholesterol
Pollaud-Chérion et al., Eur J Biochem 1998 (Second Messenger Systems) : Acetylated LDL induces rapid Ca2+ release from inositol-phosphate-sensitive Ca2+ stores mediated by pertussis-sensitive G proteins and a sustained Ca2+ rise mediated by Ca2+ influx and by Ca2+ release from ryanodine-sensitive Ca2+ stores