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miR-21 suppression prevents cardiac alterations induced by d-galactose and doxorubicin

Yihua Bei1, Xiaoting Wu2, Dragos Cretoiu3

  • 1Department of Cardiology, The First Affiliated Hospital of Nanjing Medical University, Nanjing 210029, China; Cardiac Regeneration and Ageing Lab, Experimental Center of Life Sciences, School of Life Science, Shanghai University, Shanghai 200444, China.

Journal of Molecular and Cellular Cardiology
|January 14, 2018
PubMed

Insights

Inhibition of miR-21 protects against cardiac aging caused by d-galactose and Doxorubicin. Suppressing miR-21 prevents cardiomyocyte senescence by targeting PTEN, offering a new strategy for combating heart aging.

Area of Science:

  • Cardiovascular Biology
  • Aging Research
  • Molecular Biology

Background:

  • MicroRNAs (miRNAs) are implicated in aging processes.
  • The role of miRNAs in d-galactose (d-gal) and Doxorubicin (Dox)-induced cardiac aging is not well understood.
  • Cardiac aging models are crucial for studying age-related cardiovascular diseases.

Purpose of the Study:

  • To investigate the role of dysregulated miRNAs in cardiac aging models.
  • To identify specific miRNAs involved in d-gal-induced cardiac alterations and Dox-induced cardiomyocyte senescence.
  • To explore the therapeutic potential of targeting specific miRNAs for cardiac aging.

Main Methods:

  • Utilized miRNA arrays to identify dysregulated miRNAs in aged mouse hearts.
  • Validated miRNA changes in d-gal-induced pseudo-aging mice and Dox-induced cardiomyocyte senescence models.
  • Employed quantitative reverse transcription polymerase chain reactions (qRT-PCR) for miRNA validation.
  • Assessed cardiomyocyte senescence using beta-galactosidase staining and aging gene markers.
  • Identified miR-21 targets using molecular assays and confirmed PTEN as a direct target.
  • Studied the effects of miR-21 knockout on d-gal-induced cardiac aging and function.

Main Results:

  • miR-21 expression was significantly increased in all cardiac aging models.
  • Overexpression of miR-21 promoted Dox-induced cardiomyocyte senescence, while its suppression prevented it.
  • Phosphatase and tensin homolog (PTEN) was identified as a direct target of miR-21, mediating senescence.
  • miR-21 knockout mice exhibited resistance to d-gal-induced cardiac aging markers and functional decline.

Conclusions:

  • miR-21 plays a critical role in promoting cardiac aging and cardiomyocyte senescence.
  • Inhibition of miR-21 demonstrates a protective effect against d-gal and Dox-induced cardiac damage.
  • Targeting miR-21 via PTEN inhibition presents a potential therapeutic strategy for mitigating cardiac aging.
Keywords:
DoxorubicinPhosphatase and tensin homologd-galactose-induced agingmiR-21

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