Effects of hypochlorite-modified low-density and high-density lipoproteins on intracellular Ca2+and plasma membrane Ca2+-ATPase activity of human platelets

Zabe, Martin; Feltzer, Rhona; Malle, Ernst; Sattler, Wolfgang; Dean, William L.

doi:10.1054/ceca.1999.0081

Cited by 22 publications

(14 citation statements)

References 43 publications

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“…It was however found that unmodified HDL shows only a weak protective effect against platelet activation by oxidized phospholipids. Paradoxically, the antiplatelet effect of HDL was enhanced dramatically after oxidation of HDL; the effect was found to be mediated through SR-B1 93,94) . The size of HDL particles was another characteristic to affect the ability of HDL to inhibit platelet activation: smaller HDL3 had little effect on platelet activation, while inhibition was observed by bigger apoE containing HDL2 particles 90) .…”

Section: Thrombosismentioning

confidence: 97%

Antiatherogenic Functionality of High Density Lipoprotein: How Much versus How Gooden-subtitle=

Sviridov

Mukhamedova

Remaley

et al. 2008

JAT

104

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Section: Thrombosismentioning

confidence: 97%

Antiatherogenic Functionality of High Density Lipoprotein: How Much versus How Gooden-subtitle=

Sviridov

Mukhamedova

Remaley

et al. 2008

JAT

104

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“…The highly reactive biological oxidant hypochlorous acid (HOCl) is generated via the myeloperoxidase-catalysed oxidation of the physiological concentrations of chloride (Cl -) by H 2 O 2 (Zavodnik et al 2001;Winterbourn 2002). HOCl plays an important role in both microbial killing and inflammatory tissue injury by neutrophils (Soszyński et al 2002) and has been implicated also in the diseases or pathological states like ischemia/reperfusion, atherosclerosis, skeletal muscle dysfunction, rheumatoid arthritis and in infammatory conditions Soszyński et al 2002), and is believed to participate in the development of atherosclerotic lesions (Zabe et al 1999).…”

Section: Introductionmentioning

confidence: 99%

Oxidative injury induced by hypochlorous acid to Ca-ATPase from sarcoplasmic reticulum of skeletal muscle and protective effect of trolox

Štrosová

Karlovska²,

Spickett

et al. 2009

gpb

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Abstract. Hypochlorous acid (HOCl) concentration-dependently decreased ATPase activity and SH groups of pure Ca-ATPase from sarcoplasmic reticulum (SERCA) of rabbit skeletal muscle with IC 50 of 150 µmol/l and 6.6 µmol/l, respectively. This indicates that SH goups were not critical for impairment of Ca-ATPase activity. Pure Ca-ATPase activity was analysed individually with respect to both substrates, Ca 2+

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“…n-LDL has often been oxidized in the presence of low levels of copper. 7,13,14 Copper-oxidized LDL by itself can cause strong aggregation and dense-granule secretion in washed platelets [7][8][9] However, hypochlorous acid (HOCl)-LDL has been shown to possess similar functional properties as copperoxidized LDL but with important differences 15 and may well be closest to oxidized species formed in vivo. 16 HOCl-LDL is most effective in washed platelets but will induce aggregation when used at high concentrations in platelet-rich plasma.…”

Section: Introductionmentioning

confidence: 99%

LDL oxidized by hypochlorous acid causes irreversible platelet aggregation when combined with low levels of ADP, thrombin, epinephrine, or macrophage-derived chemokine (CCL22)

Coleman

Polanowska-Grabowska

Marcinkiewicz

et al. 2004

Blood

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The in vitro oxidation of low-density lipoprotein (LDL) by hypochlorous acid produces a modified form (HOCl-LDL) capable of stimulating platelet function. We now report that HOCl-LDL is highly effective at inducing platelet function, causing stable aggregation and α-granule secretion. Such stimulation depended on the presence of low levels of primary agonists such as adenosine diphosphate (ADP) and thrombin, or others like epinephrine (EPI) and macrophage-derived chemokine (MDC, CCL22). Agonist levels, which by themselves induced little or reversible aggregation, caused strong stable aggregation when combined with low levels of HOCl-LDL. Platelet activation by HOCl-LDL and ADP (1 μM) caused P-selectin (CD62P) exposure, without serotonin or adenosine triphosphate (ATP) secretion. Intracellular calcium levels rose slowly (from 100 to 200 nM) in response to HOCl-LDL alone and rapidly when combined with ADP to about 300 nM. p38 mitogen-activated protein kinase (MAPK) became phosphorylated in response to HOCl-LDL alone. This phosphorylation was not blocked by the protein kinase C (PKC) inhibitor bisindolylmaleimide, which reduced the extent of aggregation and calcium increase. However, the p38 MAPK inhibitor SB203580 blocked platelet aggregation and phosphorylation of p38 MAPK. These findings suggest that HOCl-LDL exposed during atherosclerotic plaque rupture, coupled with low levels of primary agonists, can rapidly induce extensive and stable thrombus formation. (Blood. 2004;104:380-389)

show abstract

Effects of hypochlorite-modified low-density and high-density lipoproteins on intracellular Ca2+and plasma membrane Ca2+-ATPase activity of human platelets

Cited by 22 publications

References 43 publications

Antiatherogenic Functionality of High Density Lipoprotein: How Much versus How Gooden-subtitle=

Antiatherogenic Functionality of High Density Lipoprotein: How Much versus How Gooden-subtitle=

Oxidative injury induced by hypochlorous acid to Ca-ATPase from sarcoplasmic reticulum of skeletal muscle and protective effect of trolox

LDL oxidized by hypochlorous acid causes irreversible platelet aggregation when combined with low levels of ADP, thrombin, epinephrine, or macrophage-derived chemokine (CCL22)

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