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IL-17 Induces MPTP opening through ERK2 and P53 signaling pathway in human platelets

Jing Yuan1, Pei-Wu Ding1, Miao Yu1

  • 1Laboratory of Cardiovascular Immunology, Institute of Cardiology, Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, 430022, China.

Journal of Huazhong University of Science and Technology. Medical Sciences = Hua Zhong Ke Ji Da Xue Xue Bao. Yi Xue Ying De Wen Ban = Huazhong Keji Daxue Xuebao. Yixue Yingdewen Ban
|October 23, 2015
PubMed

Insights

The inflammatory cytokine IL-17 triggers mitochondrial permeability transition pore (MPTP) opening in platelets, leading to activation. This process involves the ERK2 and P53 signaling pathways, and can be blocked by cyclosporine-A.

Area of Science:

  • * Hematology
  • * Immunology
  • * Cell Biology

Background:

  • * Platelet activation is critical in hemostasis and thrombosis.
  • * Mitochondrial permeability transition pore (MPTP) opening is a key event in platelet activation.
  • * The specific triggers for MPTP opening during platelet activation are not fully understood.

Purpose of the Study:

  • * To investigate the role of the inflammatory cytokine Interleukin-17 (IL-17) in triggering MPTP opening during platelet activation.
  • * To elucidate the signaling pathways involved in IL-17-induced platelet activation.
  • * To determine if MPTP inhibition can attenuate IL-17 effects on platelets.

Main Methods:

  • * Measurement of mitochondrial membrane potential (ΔΨm) to assess MPTP opening.
  • * Assessment of platelet aggregation and activation markers (CD62P, PAC-1).
  • * Analysis of signaling pathway components, including ERK2 and P53 phosphorylation.
  • * Use of MPTP inhibitor cyclosporine-A (CsA) to block MPTP opening.

Main Results:

  • * IL-17 administration increased MPTP opening and reduced ΔΨm in platelets.
  • * Platelet aggregation, CD62P, PAC-1 expression, and P53/ERK2 phosphorylation were enhanced by IL-17.
  • * Cyclosporine-A (CsA) effectively attenuated the IL-17-induced platelet activation and MPTP opening.
  • * IL-17 induced MPTP opening and subsequent platelet activation via the ERK2 and P53 signaling pathway.

Conclusions:

  • * IL-17 is a significant inflammatory trigger for MPTP opening in platelets.
  • * The ERK2 and P53 signaling pathways mediate IL-17-induced platelet activation and aggregation.
  • * Inhibiting MPTP opening with CsA can counteract IL-17's pro-platelet effects.
Keywords:
IL-17cyclosporine-Amitochondrial permeability transition poreplatelet activation

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