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Platelet activation by Streptococcus sanguinis is accompanied by MAP kinase phosphorylation
Ahmed Y Abdulrehman1, Elke C G Jackson, Archibald McNicol
1Departments of Oral Biology, University of Manitoba, Winnipeg, Manitoba, Canada.
Platelets
|March 1, 2012
Summary
Oral bacteria like S. sanguinis activate platelets, triggering signaling pathways. This study reveals Erk2 MAP kinase involvement in S. sanguinis-induced platelet aggregation and phosphorylation, distinct from p38 MAP kinase.
Area of Science:
- Biochemistry
- Immunology
- Microbiology
Background:
- Infections, particularly oral bacteria, are increasingly linked to atherothrombotic conditions.
- Streptococcus sanguinis (S. sanguinis) strain 2017-78 is known to induce platelet aggregation.
- Platelet activation by S. sanguinis involves complex signaling, including protein phosphorylation and dependence on von Willebrand factor (vWF) and immunoglobulin G (IgG).
Purpose of the Study:
- To investigate the specific role of mitogen-activated protein (MAP) kinases in S. sanguinis strain 2017-78-induced platelet activation.
- To elucidate the signaling pathways downstream of S. sanguinis interaction with platelets, focusing on Erk2 and p38 MAP kinases and cPLA(2).
Main Methods:
- Immunoblotting was employed to analyze the phosphorylation status of MAP kinases (Erk2, p38) and cPLA(2) in platelets stimulated with S. sanguinis strain 2017-78.
- Platelets were pretreated with aspirin or RGDS peptide to assess their effects on signaling events.
- The p38 inhibitor SB203580 was used to evaluate the role of p38 in aggregation and phosphorylation.
Main Results:
- S. sanguinis strain 2017-78 induced a triphasic phosphorylation pattern of Erk2, similar to other signaling proteins, with rephosphorylation dependent on αIIbβ3 integrin engagement.
- Aspirin and RGDS inhibited the Erk2 rephosphorylation phase but not initial phosphorylation or dephosphorylation.
- p38 MAP kinase and cPLA(2) phosphorylation remained elevated upon S. sanguinis stimulation, unaffected by aspirin; however, the p38 inhibitor SB203580 inhibited aggregation without altering p38 or cPLA(2) phosphorylation.
Conclusions:
- The study confirms the activation of Erk2 and p38 MAP kinases, and cPLA(2) in platelets stimulated by S. sanguinis strain 2017-78.
- Erk2 appears to play a role in the cPLA(2) phosphorylation cascade during S. sanguinis-induced platelet activation.
- p38 MAP kinase is involved in S. sanguinis-induced platelet aggregation but not directly in the phosphorylation of p38 or cPLA(2).
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