Abstract

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.

Highlights

  • Traumatic injury is life threatening and it is the fourth leading cause of death in high-income countries [1, 2]

  • Exclusion criteria were patients aged less than 16 years old, pregnant women, or those who were on anticoagulant medications or had surgeries prior to attending the emergency department (ED). 15 healthy adult donors served as the control group

  • The present study showed that the plasma miR-24 level was significantly elevated in major trauma patients, especially in Trauma-induced coagulopathy (TIC) patients

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Summary

Introduction

Traumatic injury is life threatening and it is the fourth leading cause of death in high-income countries [1, 2]. Coagulation factor deficits after severe trauma have been recognized by a number of studies for many decades [9,10,11,12,13]. It is verified by the successful therapies of repletion of clotting factors by infusion of higher ratio of flesh frozen plasma (FFP) and additional prothrombin complex concentrate (PCC) in trauma patients [14,15,16]. 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 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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