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Microfluidics in Assessing Platelet Function
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Comprehensive characterization of platelet function in dogs with hyperadrenocorticism.

Sanggu Kim1, Dohee Lee2, Preeti Kumari Chaudhary1

  • 1Laboratory of Veterinary Pathology and Platelet Signaling, College of Veterinary Medicine, Chungbuk National University, Cheongju.

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|February 6, 2025
PubMed
Summary

Hyperadrenocorticism (HAC) impairs platelet function in dogs, reducing aggregation and secretion. Excessive cortisol suppresses thromboxane A2 generation via ERK and AKT pathways, impacting hemostasis.

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Area of Science:

  • Veterinary Medicine
  • Hematology
  • Endocrinology

Background:

  • Hyperadrenocorticism (HAC) is linked to hypercoagulability and thromboembolic disease risk in humans and dogs.
  • Platelets are crucial for thrombosis and hemostasis, but their function in HAC dogs remains uncharacterized.

Purpose of the Study:

  • To investigate platelet function and its molecular mechanisms in dogs with HAC.
  • To compare platelet responses between dogs with HAC and healthy controls.

Main Methods:

  • Prospective cross-sectional study involving 7 dogs with HAC and 15 healthy dogs.
  • Evaluation of platelet aggregation, dense-granule secretion, and thromboxane A2 generation.
  • Analysis of ERK and AKT phosphorylation in response to thrombin.

Main Results:

  • Platelet aggregation and secretion induced by 2-MeSADP and thrombin were significantly reduced in HAC dogs.
  • Prednisolone inhibited platelet function in normal dogs but not in HAC dogs, indicating cortisol's role.
  • A negative correlation was observed between platelet aggregation and post-ACTH cortisol levels.
  • Thromboxane A2 generation and ERK/AKT phosphorylation were suppressed in HAC dogs.

Conclusions:

  • Excessive cortisol in canine HAC negatively impacts platelet function.
  • Cortisol suppresses thromboxane A2 generation by regulating ERK and AKT phosphorylation.
  • These findings elucidate a molecular mechanism for altered hemostasis in canine HAC.