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Impaired mobilization of intracellular calcium in neonatal platelets
1Department of Pediatrics, Temple University School of Medicine, Philadelphia, Pennsylvania, USA.
Insights
Neonatal platelets show impaired calcium release, a key factor in platelet dysfunction. This study used Fura-2 to measure calcium levels, revealing significantly lower responses to collagen and thrombin in newborns compared to adults.
Area of Science:
- Hematology
- Neonatal Physiology
- Cellular Biology
Background:
- Neonatal platelets exhibit functional abnormalities, including impaired aggregation and release reactions.
- Calcium ions are critical mediators of platelet activation and function.
Purpose of the Study:
- To investigate calcium mobilization in neonatal platelets.
- To determine if impaired calcium release contributes to neonatal platelet dysfunction.
Main Methods:
- Umbilical cord blood from healthy, full-term neonates was used.
- Cytoplasmic calcium levels were measured using the fluorescent probe Fura-2.
- Platelets were stimulated with collagen or thrombin to assess calcium release.
Main Results:
- Neonatal platelets demonstrated significantly impaired intracellular calcium release in response to collagen and thrombin compared to adult controls.
- Calcium release was reduced by over 50% for collagen and nearly 50% for thrombin in neonates versus adults.
- The calcium content of the dense tubular system was normal, ruling out reduced calcium stores as the cause.
Conclusions:
- Impaired calcium mobilization is a primary cause of the functional abnormalities observed in neonatal platelets.
- This dysfunction is not due to a lack of intracellular calcium stores but rather an issue with calcium release mechanisms.
Abstract:
Abnormalities in platelet functions including aggregation and the release reaction have long been recognized to be present in neonatal platelets. Because calcium is an important mediator of many platelet functions, we have investigated the mobilization of calcium in neonatal platelets. All umbilical cord blood samples were obtained from healthy, full term gestations. Changes in cytoplasmic calcium levels were monitored using Fura-2 as a fluorescent probe. Fura-2-loaded washed platelets were stimulated with the agonists collagen (2 micrograms/mL) or thrombin (1.0 U/mL). When compared with adult controls, intracellular calcium release in the platelets of the neonate was significantly impaired in response to these agonists. Mean levels for calcium release in adults versus neonates in response to collagen were 168 +/- 120 nM (+/-SD, n = 10), and 61 +/- 69 nM (n = 7, p < 0.05). A decrease in response to thrombin was also observed [1296 +/- 503 nM (n = 8) in adults versus 603 +/- 482 nM (n = 7) in neonates, p < 0.025]. Results similar to those observed with unpaired neonatal and adult platelets were also obtained when neonatal platelets (n = 5) were compared with their paired maternal controls. In further studies, we have documented that the calcium content of the dense tubular system was normal in the neonatal platelet, indicating that the observed impairment in calcium mobilization in the neonate was not due to a decrease in calcium stores. The previously documented abnormalities in neonatal platelet function appear to be due to the impaired mobilization of this important intracellular mediator.