What question did this study set out to answer?

To understand how platelet CD36 signaling activates downstream pathways that promote procoagulant activities and fibrin deposition.

October 31, 2018Blood AdvancesOpen Access

Platelet CD36 signaling through ERK5 promotes caspase-dependent procoagulant activity and fibrin deposition in vivo

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To understand how platelet CD36 signaling activates downstream pathways that promote procoagulant activities and fibrin deposition.
Evaluated platelet responses to oxidized low-density lipoprotein (oxLDL) using pharmacologic inhibitors.
Observed interactions of CD36, ERK5, and caspases in platelet signaling pathways.
Utilized in vivo models with apoE-null hyperlipidemic mice to study arterial thrombosis.
OxLDL exposure on platelets significantly increases phosphatidylserine (PSer) levels and fibrin generation.
Caspase activity is essential for PSer exposure and was inhibited by blocking CD36 and ERK5 signaling.
In vivo models showed decreased fibrin accumulation in mice lacking ERK5 or CD36 under hyperlipidemic conditions.

Structured PICO

Population

apoE-null hyperlipidemic mice on high-fat diet and isolated platelets

Intervention

Inhibition or genetic deletion of CD36, ERK5, or caspases

Comparator

Untreated controls, wild-type mice, or chow diet-fed animals

Outcome

Phosphatidylserine (PSer) exposure and arterial fibrin accumulation upon vessel injurysurrogate

Platelet signaling through CD36 and ERK5 induces a procoagulant phenotype in hyperlipidemic environments by enhancing caspase-mediated phosphatidylserine exposure.

Discussion

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Implication

CD36-ERK5 signaling may promote fibrin deposition in hyperlipidemia; hypothesis-generating for antithrombotic targets pending human studies.

Cite This Study

Yang et al. (2018) studied this question.

synapsesocial.com/papers/6a1bab470ea968f653ac14de https://doi.org/10.1182/bloodadvances.2018025411

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Implication

CD36-ERK5 signaling may promote fibrin deposition in hyperlipidemia; hypothesis-generating for antithrombotic targets pending human studies.

Platelet CD36 signaling through ERK5 promotes caspase-dependent procoagulant activity and fibrin deposition in vivo

Key Points

Structured PICO

Discussion

Implication

Cite This Study

Platelet CD36 signaling through ERK5 promotes caspase-dependent procoagulant activity and fibrin deposition in vivo

Key Points

Structured PICO

Discussion

Implication

Cite This Study

Also Consider

Also Consider