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Updated: Jun 13, 2026

Isolation of Endothelial Progenitor Cells from Human Umbilical Cord Blood
Published on: September 14, 2017
Potential link between C3a, C3b and endothelial progenitor cells in resistant hypertension
Eli Magen1, Arie Feldman, Ziona Cohen
1Medicine B Department, Barzilai Medical Center, Ben Gurion University of Negev, Ashkelon, Israel. allergologycom@gmail.com
Introduction:
Endothelial progenitor cells (EPC) and complement C3 are involved in the pathophysiology of arterial hypertension. C3a is the negative regulator of progenitor cells egress during their mobilization from bone marrow. Previously, higher plasma concentration of C3 was observed in resistant arterial hypertension (RAH) than in controlled arterial hypertension (CAH). Thus, we hypothesized that RAH would be associated with complement C3 activation and reduced number of circulating EPCs.
Objective:
To compare C3a, C3b and their correlation with circulating EPC in subjects with RAH and CAH.
Methods:
Blood pressure was measured by electronic sphygmomanometer. EPCs were identified as CD34+/CD133+/KDR+ cells by flow cytometry. C3a and C3b were determined using enzyme-linked immunosorbent assay (Quidel, CA).
Results:
: RAH group (n = 20) and CAH group (n = 20) and 17 healthy individuals (control group) were recruited. In the RAH group, C3a (858.1 +/- 70.6 microg/dL) was higher than in the CAH group (816.1 +/- 123.3 microg/dL; P < 0.001), and in the control group (751.3 +/- 98.8; P < 0.001), C3b (564.1 +/- 54.7 microg/dL) was higher than in the CAH group (490.2 +/- 58.5 microg/dL; P < 0.001). In control group (456.3 +/- 98.8; P < 0.001), statistically significant negative correlation was observed between C3a and blood levels of EPC (r = -0.523, P = 0.018); statistically significant positive correlation was observed between systolic blood pressure and blood levels of C3a (r = 0.52, P = 0.02) and between systolic blood pressure and blood levels of C3b (r = 0.57, P = 0.009).
Conclusion:
RAH is characterized by higher levels of C3 component fragments and a negative correlation between circulating C3a and EPCs.
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