• Users Online: 657
  • Print this page
  • Email this page
Year : 2018  |  Volume : 2  |  Issue : 2  |  Page : 136-141

Analysis of endothelial progenitor subpopulation cells, oxidative DNA damage, and their role in coronary artery disease

Laboratory of Genetics and Stem Cell Biology, Advanced Research Centre, Narayana Medical College and Hospital, Nellore, Andhra Pradesh, India

Correspondence Address:
Dr. Mahaboob Vali Shaik
Laboratory of Genetics and Stem Cell Biology, Advanced Research Centre, Narayana Medical College and Hospital, Nellore - 524 001, Andhra Pradesh
Login to access the Email id

Source of Support: None, Conflict of Interest: None

DOI: 10.4103/bbrj.bbrj_41_18

Rights and Permissions

Background: Endothelial dysfunction has been associated for the cause of atherosclerosis or cardiovascular diseases (CVDs). Endothelial progenitor cells (EPCs) are exposed to oxidative stress during vascular injury as residents of blood vessel walls or as circulating cells homing to the sites of neovascularization. The current study was designed to analyze various subpopulations of EPCs and their DNA damage in CVDs. Methods: The study included 50 coronary artery disease (CAD) patients which was confirmed by angiography and 50 age-matched healthy controls without CAD. Flow cytometric analysis performed to measure subpopulations in EPCs in the peripheral blood using markers such as CD34, CD133, VEGFR2, and CD45. Oxidative DNA damage was analyzed in CD34+ cells. Mean EPC count was expressed as a percentage of total white blood cells. Three different subpopulations with CD45−/CD133+/VEGFR2+, CD45−/CD34+/VEGFR2+, and CD45−/CD34+/CD133+ coexpressions were measured with various percentages. Results: Subpopulation of CD45−/CD34+/VEGFR2+ cells had shown significant (P = 0.001) decrease in CAD patients in comparison with the healthy controls. There was no significant difference in the subpopulations of CD45−/CD34+/CD133+ cells (P = 0.005) and CD45−/CD133+/VEGFR2+ cells (P = 0.005) in CAD and healthy controls. The CD45−/CD34+/VEGFR2+ subpopulation EPC showed positive correlation with the severity of coronary stenosis (r = 0.35, P = 0.026), while other EPC subpopulation count did not show any correlation. Oxidative DNA damage was higher in CAD compared with controls. The number of EPC subpopulation CD45−/CD34+/VEGFR2+ was inversely correlated with oxidative DNA damage (P = 0.001), hypertension (P = 0.001), and diabetes mellitus (P = 0.004). Conclusion: We observed an association between CD45−/CD34+/VEGFR2 subpopulation EPCs and DNA damage in CAD condition. These findings support a cell biologist in searching the role of EPC populations in the pathophysiology or diagnosis of the disease by a clinician.

Print this article     Email this article
 Next article
 Previous article
 Table of Contents

 Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
 Related articles
 Citation Manager
 Access Statistics
 Reader Comments
 Email Alert *
 Add to My List *
 * Requires registration (Free)

 Article Access Statistics
    PDF Downloaded234    
    Comments [Add]    
    Cited by others 2    

Recommend this journal