Overexpression of miR-24 Is Involved in the Formation of Hypocoagulation State after Severe Trauma by Inhibiting the Synthesis of Coagulation Factor X
Background. Dysregulation of microRNAs may contribute to the progression of trauma-induced coagulopathy (TIC). We aimed to explore the biological function that miRNA-24-3p (miR-24) might have in coagulation factor deficiency after major trauma and TIC. Methods. 15 healthy volunteers and 36 severe tr...
Main Authors: | , , , , |
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Format: | Article |
Language: | English |
Published: |
Hindawi Limited
2017-01-01
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Series: | Disease Markers |
Online Access: | http://dx.doi.org/10.1155/2017/3649693 |
Summary: | Background. Dysregulation of microRNAs may contribute to the progression of trauma-induced coagulopathy (TIC). We aimed to explore the biological function that miRNA-24-3p (miR-24) might have in coagulation factor deficiency after major trauma and TIC. Methods. 15 healthy volunteers and 36 severe trauma patients (Injury Severity Score ≥ 16 were enrolled. TIC was determined as the initial international normalized ratio >1.5. The miR-24 expression and concentrations of factor X (FX) and factor XII in plasma were measured. In vitro study was conducted on L02 cell line. Results. The plasma miR-24 expression was significantly elevated by 3.17-fold (P=0.043) in major trauma patients and reduced after 3 days (P<0.01). The expression level was significantly higher in TIC than in non-TIC patients (P=0.040). Multivariate analysis showed that the higher miR-24 expression was associated with TIC. The plasma concentration of FX in TIC patients was significantly lower than in the non-TIC ones (P=0.030) and controls (P<0.01). A negative correlation was observed between miR-24 and FX. miR-24 transduction significantly reduced the FX level in the supernatant of L02 cells (P=0.030). Conclusions. miR-24 was overexpressed in major trauma and TIC patients. The negative correlation of miR-24 with FX suggested the possibility that miR-24 might inhibit the synthesis of FX during TIC. |
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ISSN: | 0278-0240 1875-8630 |