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Fibrinolysis-resistant carbonylated fibrin detected in thrombi attached to the vascular wall of abdominal aortic aneurysms. | LitMetric

AI Article Synopsis

  • The study explored how acrolein alters fibrinogen, impacting its role in promoting fibrinolysis and leading to the creation of fibrinolysis-resistant fibrin clots.
  • Acrolein-modified fibrinogen showed increased resistance to breakdown during fibrinolysis assays, with specific lysine carbonylation linked to slower clot lysis.
  • The findings suggest that this acrolein-induced modification may contribute to long-lasting thrombi in conditions like abdominal aortic aneurysms, highlighting the potential clinical significance of these mechanisms.

Article Abstract

In this study, we investigated how carbonylation of fibrinogen by acrolein modified its indispensable function to enhance fibrinolysis after being converted to fibrin and contributed to generating a fibrinolysis-resistant fibrin clot. Acrolein-treated fibrinogen was subjected to tissue plasminogen activator-induced fibrinolysis assay and the effect of lysine residue carbonylation in fibrinogen on fibrinolysis was analyzed. The acrolein-treated fibrinogen-derived fibrin clot appeared more resistant to fibrinolysis and the N-acetyl 3-formyl-3,4-dehydropiperidino (FDP)-Lysine levels in the lysed solution were positively correlated with the duration of clot lysis. The lysine analog 6-amino hexanoic acid (6AHA), which mimics the C-terminal lysine of fibrin, was carbonylated and its enhancing effect on Glu-plasminogen activation was evaluated. After incubation with acrolein, 6AHA was converted to N-acetyl FDP-6AHA, losing its ability to enhance Glu-plasminogen activation. These results suggest that fibrinogen carbonylation by acrolein to generate N-acetyl FDP-Lysine resulted in the generation of fibrinolysis-resistant fibrin by attenuating the C-terminal lysine-dependent activation of the Glu-plasminogen. In abdominal aortic aneurysms, fibrin(ogen) containing the acrolein adduct N-acetyl FDP-Lysine was detected in the vascular wall-attached thrombi. These results suggest that this mechanism is likely involved in the modification of fibrinolysis-resistant thrombi and to their persistence for a long period.

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Source
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7691368PMC
http://dx.doi.org/10.1038/s41598-020-77582-1DOI Listing

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