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Oxidative Versus Thrombotic Stimulation of Platelets Differentially activates Signalling Pathways.

Pouran Karimi1, Nadereh Rashtchizadeh

  • 1Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz, Iran.

Journal of Cardiovascular and Thoracic Research
|November 20, 2013
PubMed
Summary

Oxidized low-density lipoprotein (OxLDL) and thrombin activate platelets by increasing mitogen-activated protein kinases (MAPKs) and P-selectin expression. MAPK inhibitors reduced these effects, suggesting potential for treating atherosclerosis.

Keywords:
AtherosclerosisC-Jun N-terminal Kinase ExtracellularP-selectinP38-Mitogen Activated Protein KinaseSignal-regulated Kinase

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Area of Science:

  • Cardiovascular biology
  • Platelet signaling
  • Atherosclerosis research

Background:

  • Atherosclerosis is an inflammatory disease linked to oxidative stress and thrombosis.
  • Platelets play a key role in atherothrombotic events.
  • Oxidized low-density lipoprotein (OxLDL) and thrombin are implicated in platelet activation.

Purpose of the Study:

  • To investigate the role of OxLDL and thrombin in activating mitogen-activated protein kinases (MAPKs) in human platelets.
  • To determine the effect of OxLDL and thrombin on P-selectin expression in platelets.
  • To evaluate the potential of MAPK inhibitors in mitigating OxLDL- and thrombin-induced platelet activation.

Main Methods:

  • Human platelets were treated with OxLDL and thrombin.
  • Phosphorylation of P38MAPK, JNK, and ERK1/2 was measured using ELISA.
  • P-selectin expression was quantified via ELISA.
  • Specific MAPK inhibitors (SB203580, PD980559, SP6000125) were used to assess their effects.

Main Results:

  • OxLDL and thrombin significantly increased P-selectin expression and phosphorylation of P38MAPK, JNK, and ERK1/2 in platelets.
  • Inhibitors of P38MAPK and JNK significantly reduced P-selectin expression in platelets activated by both OxLDL and thrombin.
  • ERK1/2 phosphorylation was also induced but not significantly affected by its specific inhibitor in this context.

Conclusions:

  • MAPK signaling pathways are involved in OxLDL- and thrombin-induced platelet activation and P-selectin expression.
  • MAPK inhibitors demonstrate potential in reducing atherothrombotic events.
  • Targeting MAPK pathways may offer a therapeutic strategy for inhibiting atherosclerosis development.