SAMD1 attenuates antiphospholipid syndrome-induced vascular injury and pregnancy complications

SAMD1 may reduce APS-induced vascular injury and embryo loss by regulating cellular senescence, proliferation, migration, and angiogenesis.

The expression of SAMD1 in APS patients and healthy controls was detected by quantitative real-time polymerase chain reaction (qRT-PCR). Anti-B2 GPI and anticardiolipin antibody (ACA) levels were tested by enzyme-linked immunosorbent assay, MMP-9, iNOS, ICAM-1, and MCP-1 mRNA and protein levels determined by qRT-PCR and Western blot, cellular senescence detected by β-galactosidase staining, cell proliferation ability detected by CCK-8 assay, cell viability detected by trypan blue staining, cell mobility detected by Transwell, and cell angiogenesis ability detected by matrigel tube formation assay. An APS pregnant mouse model was constructed, and the embryo absorption rate was calculated.

This study was intended to investigate the effect of SAMD1 on antiphospholipid syndrome (APS)-induced vascular injury in human umbilical vein endothelial cells (HUVECs) and pregnancy complications in mice.

SAMD1 expression was low in serum of APS patients, which was correlated with the history of thrombosis and the number of adverse pregnancies. Anti-B2 GPI and ACA levels were increased in APS. The expressions of MMP-9, iNOS, ICAM-1, and MCP-1 were also significantly upregulated in HUVECs treated with APS serum. APS promoted HUVEC senescence and inhibited cell proliferation, migration, and angiogenesis. Overexpression of SAMD1 reversed the above results. Experiments on the APS pregnant mouse model confirmed that overexpression of SAMD1 reduced the rate of fetal loss.