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Updated: Jul 27, 2026
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Turbidimetry on Human Washed Platelets: The Effect of the Pannexin1-inhibitor Brilliant Blue FCF on Collagen-induced Aggregation
Published on: April 6, 2017
Deficient collagen-induced activation in the newborn platelet.
S J Israels1, M Daniels, E M McMillan
1Manitoba Institute of Cell Biology, University of Manitoba, Winnipeg, Canada.
Pediatric Research
|April 1, 1990
Summary
Neonatal platelets exhibit normal responses to thrombin but impaired secretion when activated by collagen. This suggests specific defects in the collagen pathway, not a general platelet dysfunction in newborns.
Area of Science:
- Hematology
- Platelet Biology
- Neonatal Physiology
Background:
- Neonatal platelets play a crucial role in hemostasis.
- Understanding neonatal platelet function is vital for assessing bleeding risks.
Purpose of the Study:
- To investigate the impaired secretion response in neonatal platelets.
- To compare neonatal and adult platelet activation pathways.
Main Methods:
- Compared washed neonatal and adult platelets using thrombin, collagen, and specific activators.
- Assessed platelet aggregation, serotonin secretion, and protein phosphorylation.
- Evaluated collagen-platelet interaction via adhesion assays and flow cytometry for GPIa/IIa receptor presence.
- Measured phosphoinositide hydrolysis and arachidonic acid release.
Main Results:
- Neonatal platelets showed no impairment in response to thrombin, inositol trisphosphate, or oleoyl-acetyl glycerol.
- A markedly decreased response to collagen was observed in neonatal platelets.
- Platelet adhesion to collagen and GPIa/IIa receptor expression were similar between neonatal and adult platelets.
- Phosphoinositide hydrolysis was reduced in response to collagen but normal with thrombin in neonatal platelets.
- Arachidonic acid release was higher with thrombin but lower with collagen in neonatal platelets compared to adults.
Conclusions:
- Neonatal platelet secretion is specifically impaired in response to collagen, not due to general dysfunction.
- The collagen activation pathway, particularly phosphoinositide hydrolysis, appears deficient in neonatal platelets.
- Adhesion and GPIa/IIa receptor expression are not the cause of the impaired collagen response.
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