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Complement Factors C3a and C5a Contribute to Angiogenic Imbalance in Preeclampsia

Although recent evidence from our lab and others suggests increases in circulating concentrations of complement activation products C3a and C5a play a key role in pathogenesis of preeclampsia, the exact role they play in disease progression remains unclear. We hypothesized complement factors C3a and C5a would stimulate production of anti‐angiogenic factors (sEng) and decrease production of pro‐angiogenic factors (PlGF) from placental and endothelial cells. BeWo trophoblast cells and endothelial cells (HUVECs) were cultured in complete cell media for 2 hr with 10 and 100 nM C3a or C5a in culture media at three oxygen concentrations (20%, 8%, and 1.5%). sEng and PlGF were measured in culture media by ELISA. Treatment of HUVECS with C3a and C5a significantly decreased sEng production (p < 0.05). C3a increased PlGF (p < 0.05), while C5a decreased PlGF (p < 0.05). BeWo cells treated with 100 nM C5a increased sEng production (p < 0.05). Angiogenesis was measured by determining endothelial cell tube formation in HUVECs exposed to C3a or C5a for 8 hr. C5a at 100 nM completely prevented tube formation (p < 0.01). The present data indicate C3a and C5a may have opposing actions in placental and endothelial cells. In addition, C5a may be the key product of complement system activation responsible for production of circulating anti‐angiogenic factors.