4.4 Article

Photobiomodulation therapy's effects on cardiac fibrosis activation after experimental myocardial infarction

期刊

LASERS IN SURGERY AND MEDICINE
卷 54, 期 6, 页码 883-894

出版社

WILEY
DOI: 10.1002/lsm.23544

关键词

cardiac remodeling; fibrosis; gene expression; myocardial infarction; photobiomodulation therapy

资金

  1. Conselho Nacional de Desenvolvimento Cientifico e Tecnologico [304607/2018-5, 308067/2014-2, 312381/2021-2]
  2. Fundacao de Amparo a Pesquisa do Estado de Sao Paulo [2012/15808-0]

向作者/读者索取更多资源

This study aimed to assess the temporal effects of Photobiomodulation therapy (PBMT) on cardiac fibrosis activation after myocardial infarction (MI) in rats. The results suggest that PBMT can interfere in cardiac fibrosis activation after MI by reversing the signaling pathway of profibrotic genes, through modulation of gene transcription and miRNA expressions.
Introduction Ischemic heart disease is the leading cause of death worldwide, and interventions to reduce myocardial infarction (MI) complications are widely researched. Photobiomodulation therapy (PBMT) has altered multiple biological processes in tissues and organs, including the heart. Objectives This study aimed to assess the temporal effects of PBMT on cardiac fibrosis activation after MI in rats. In this proof-of-concept study, we monitored the change in expression patterns over time of genes and microRNAs (miRNAs) involved in the formation of cardiac fibrosis post-MI submitted to PBMT. Materials and Methods Experimental MI was induced, and PBMT was applied shortly after coronary artery ligation (laser light of wavelength 660 nm, 15 mW of power, energy density 22.5 J/cm(2), 60 seconds of application, irradiated area 0.785 cm(2), fluence 1.1 J/cm(2)). Ventricular septal samples were collected at 30 minutes, 3, 6, 24 hours, and 3 days post-MI to determine temporal PBMT's effects on messenger RNA (mRNA) expression associated with cardiac fibrosis activation and miRNAs expression. Results PBMT, when applied after ischemia, reversed the changes in mRNA expression of myocardial extracellular matrix genes induced by MI. Surprisingly, PBMT modified cardiac miRNAs expression related to fibrosis replacement in the myocardium. Expression correlations between myocardial mRNAs were assessed. The correlation coefficient between miRNAs and target mRNAs was also determined. A positive correlation was detected among miR-21 and transforming growth factor beta-1 mRNA. The miR-29a expression negatively correlated to Col1a1, Col3a1, and MMP-2 mRNA expressions. In addition, we observed that miR-133 and Col1a1 mRNA were negatively correlated. Conclusion The results suggest that PBMT, through the modulation of gene transcription and miRNA expressions, can interfere in cardiac fibrosis activation after MI, mainly reversing the signaling pathway of profibrotic genes.

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