SDF1 gradient associates with the distribution of c-Kit+ cardiac cells in the heart

Outi Renko1, Anna-Maria Tolonen1, Jaana Rysä2

  • 1Research Unit of Biomedicine, Department of Pharmacology and Toxicology, University of Oulu, Oulu, Finland.

Scientific Reports
|January 20, 2018
PubMed

Insights

Adult cardiac stem cells (CSCs) expressing c-Kit are key for heart repair. Stromal cell-derived factor 1 alpha (SDF1α) upregulation after heart attack promotes CSC migration to injured areas, offering therapeutic potential.

Area of Science:

  • Cardiovascular Biology
  • Stem Cell Biology
  • Regenerative Medicine

Background:

  • Adult cardiac stem cells (CSCs), particularly c-Kit positive cells, are crucial for cardiac regeneration.
  • Chemokines are known to influence stem cell migration and homing.
  • Understanding molecular targets is essential for modulating endogenous CSC mobility.

Purpose of the Study:

  • To investigate molecular targets for modulating the mobility of endogenous cardiac stem cells (CSCs).
  • To explore the role of stromal cell-derived factor 1 alpha (SDF1α) in CSC redistribution after myocardial infarction.

Main Methods:

  • Experimental acute myocardial infarction (AMI) was induced in Sprague-Dawley rats.
  • Cardiac stem cells (CSCs) expressing c-Kit were tracked over a four-week follow-up period.
  • Expression levels of SDF1α and the correlation with c-Kit+ CSCs were analyzed. In vitro migration assays were performed.

Main Results:

  • Following AMI, c-Kit+ CSCs redistributed within the heart, decreasing in the atrial niche and increasing in the left ventricle and apex.
  • Increased expression of SDF1α was observed in the injured heart.
  • A significant positive correlation was found between c-Kit+ CSC numbers and SDF1α expression.
  • SDF1 treatment induced the migratory capacity of isolated c-Kit+ CSCs in vitro.

Conclusions:

  • Upregulation of SDF1α post-AMI is associated with the increased presence of endogenous c-Kit+ CSCs in the injured cardiac area.
  • SDF1α plays a role in inducing the migration of c-Kit+ CSCs towards the site of injury.
  • Targeting SDF1α may represent a therapeutic strategy to enhance cardiac repair by recruiting endogenous CSCs.

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