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Cardiac MicroRNA Expression Profile After Experimental Brain Death Is Associated With Myocardial Dysfunction and Can

Ludmila Rodrigues Pinto Ferreira1,2, Cristiano Jesus Correia3, Fernando Luiz Zanoni3

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Transplantation
|April 16, 2021
PubMed
Summary

Brain death (BD) causes cardiac microRNA (miRNA) changes linked to organ damage. Hypertonic saline solution (HSS) treatment may preserve heart function by regulating these miRNAs, suggesting potential for improved organ quality.

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Area of Science:

  • Cardiovascular Research
  • Molecular Biology
  • Transplantation Science

Background:

  • Brain death (BD) induces systemic inflammation, potentially impairing transplanted organ quality.
  • Cardiac microRNAs (miRNAs) play roles in myocardial function and may be altered by BD.
  • Hypertonic saline solution (HSS) is a potential therapeutic agent to mitigate BD-induced damage.

Purpose of the Study:

  • To investigate cardiac miRNA expression profiles following BD.
  • To correlate miRNA changes with myocardial dysfunction after BD.
  • To assess the impact of HSS treatment on cardiac miRNAs and function in BD.

Main Methods:

  • Wistar rats underwent sham-operation (SHAM) or BD, with or without HSS treatment.
  • Left ventricular (LV) pressure-volume analysis assessed cardiac function for 6 hours.
  • Screening of 641 rodent miRNAs identified differentially expressed cardiac miRNAs; computational analysis explored targets and pathways.

Main Results:

  • BD induced enhanced expression of pathways related to inflammation and myocardial apoptosis.
  • Two miRNAs, miR-30a-3p and miR-467f, correlated with LV dysfunction post-BD.
  • HSS treatment in BD and SHAM groups showed similar pathways related to heart homeostasis, with no significant LV function changes.

Conclusions:

  • Cardiac miRNAs show potential as biomarkers for assessing BD donor heart damage.
  • miRNA profiles can monitor therapeutic effects, such as HSS treatment, on organ quality.
  • Further investigation is needed on the role of BD-induced miRNAs in allograft function.