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Measurement of Factor V Activity in Human Plasma Using a Microplate Coagulation Assay
Published on: September 9, 2012
Real-time quantitative PCR analysis of factor XI mRNA variants in human platelets.
A Podmore1, M Smith, G Savidge
1The Haemophilia Center, St Thomas' Hospital, Lambeth Palace Road, London, UK.
Journal of Thrombosis and Haemostasis : JTH
|October 1, 2004
Summary
Platelets do not contain an alternatively spliced form of coagulation factor XI (FXI) mRNA. This finding resolves controversy regarding FXI variants and bleeding tendencies in FXI deficiency.
Area of Science:
- Hematology
- Molecular Biology
- Genetics
Background:
- Coagulation factor XI (FXI) is crucial for blood clotting.
- FXI deficiency presents variable bleeding, potentially due to platelet-associated FXI.
- The nature of platelet FXI is debated, with conflicting reports on an alternatively spliced variant lacking exon V.
Purpose of the Study:
- To investigate the presence and nature of FXI mRNA in platelets.
- To resolve the controversy surrounding an alternatively spliced FXI variant in platelets.
Main Methods:
- Real-time quantitative RT-PCR was used to analyze RNA from FXI-deficient patients' platelets.
- RNA was isolated from platelets of both normal and FXI-deficient individuals.
Main Results:
- FXI mRNA in platelets of both normal and FXI-deficient individuals was identical to liver mRNA.
- No evidence of an exon V deleted splice variant of FXI mRNA was detected in platelets.
Conclusions:
- Platelet FXI mRNA is not alternatively spliced.
- An unusual FXI protein cannot be produced through alternative splicing in platelets.
- This study clarifies the molecular basis of bleeding variability in FXI deficiency.
