Diabetes mellitus impairs CD133+ progenitor cell function after myocardial infarction

Area of Science:

• Cardiovascular Research
• Stem Cell Biology
• Diabetology

Background:

• Circulating progenitor cells (PC) aid in healing ischemic heart tissue.
• Diabetes mellitus (DM) may negatively impact PC number and recruitment.
• CD133(+) progenitor cells are crucial for myocardial healing and potential cell therapy.

Purpose of the Study:

• To investigate the effect of type 2 diabetes mellitus (T2DM) on CD133(+) progenitor cells (PC) in patients with acute myocardial infarction (AMI).
• To compare the number, phenotype, and function of CD133(+)PC in diabetic versus non-diabetic AMI patients.

Main Methods:

• Assessed CD133(+)PC number and phenotype via flow cytometry in AMI patients with/without T2DM and stable coronary artery disease (CAD) controls.
• Evaluated CD133(+)PC chemotaxis towards vascular endothelial growth factor (VEGF).
• Measured antioxidant enzyme expression (e.g., catalase) in CD133(+)PC using reverse-transcriptase PCR.

Main Results:

• Non-diabetic AMI patients showed increased CD133(+)PC numbers on day 3 post-AMI; diabetic patients did not.
• Enhanced chemotaxis towards VEGF was observed in both groups, but functional activation was weaker in T2DM patients.
• CD133(+)PC from T2DM patients exhibited lower catalase expression, indicating reduced antioxidant capacity.

Conclusions:

• T2DM significantly reduces the abundance and activation of CD133(+) progenitor cells following AMI.
• Impaired CD133(+)PC function in T2DM may stem from lower resistance to oxidative stress.
• These findings offer a potential explanation for delayed vascular healing and myocardial recovery in diabetic patients post-AMI.