Effect of hydroxychloroquine on antiphospholipid antibodies-inhibited endometrial angiogenesis.

BACKGROUND

Antiphospholipid syndrome (APS) is an autoimmune disease characterized by thrombotic events and/or pregnancy morbidity (≥3 recurrent early miscarriage or fetal death or a prematurity <34 weeks of gestation) with persistently positive antiphospholipid antibodies (aPLs). It is reported that aPLs damage the placental tissue by binding to β2-glycoprotein I (β2GPI) on the surface of trophoblast and endothelial cells. Hydroxychloroquine (HCQ) is considered to be beneficial in the treatment of obstetrical APS and shown to restore the aPL-inhibited invasion and differentiation of trophoblast. However, not enough evidence exists regarding the effect of HCQ on endometrial angiogenesis. The aim of our study was to assess whether HCQ has an effect on aPL-inhibited endothelial angiogenesis.

METHODS

In this research, to explore the effect of HCQ for angiogenesis, we investigated: (1) Human umbilical vein endothelial cells (HUVECs) viability by CCK-8; (2) HUVECs migration by wound healing; (3) HUVEC angiogenesis by Matrigel assay ; (4) mRNA expression of and by real-time quantitative Polymerase Chain Reaction (RT-PCR); (5) protein expression of VEGF, MMP-2 by western blot.

RESULTS

We found that HCQ treatment significantly restored the expression of aPL-inhibited and . HCQ restored aPL-inhibited HUVEC proliferation, migration, and angiogenesis .

CONCLUSION

In conclusion, aPLs inhibit HUVECs angiogenesis, however, HCQ can restore the effect of aPL-inhibited HUVECs migration and angiogenesis , demonstrating its beneficial therapeutic role in obstetrical APS.