Atherosclerosis and recurrent pregnancy losses: Common biomarkers involved?

Background and Aims : The occurrence of recurrent pregnancy losses (RPL) in women patients can be due to placental lesions such as atherosis (ATS), a vascular change similar to atherosclerosis (ATH). Women vulnerable to RPL are at higher risk of ATH and women with a family history of ATH have a predisposition to have pregnancy loss. These data underline the existence of potential common biomarkers to these two pathologies. Thus, the aim of this study is to identify the biomarkers of RPL linked to ATH in order to understand the vascular molecular processes of RPL and to offer personalized therapy in the future.Methods: A human monoclonal antibody named P3, selected for its specificity against the galectin 3 protein (Gal3) over expressed in atheroma, was tested on human placental biopsies from RPL and compared with a control group of placentas obtained from normal childbirth. For the histological characterization of placental lesions, placental biopsies were stained with hematoxylin and eosin. The bio-reactivity of P3 was tested by immunohistochemistry and the staining was quantified using imageJ software. To identify P3 target in placental protein extracts, immunoprecipitations were performed and the eluates were analyzed by western blot followed by proteomics studies to validate gal3 as the placental P3 target.Results: highlight P3 bio-reactivity on placenta with a staining 3.8-fold higher in pathological placentas compared to controls.Conclusions: These results hold great promise for the choice of galectin 3 as biomarker for atherosis and the use of P3 antibody for the prevention and therapy of recurrent pregnancy losses Background and Aims : The occurrence of recurrent pregnancy losses (RPL) in women patients can be due to placental lesions such as atherosis (ATS), a vascular change similar to atherosclerosis (ATH). Women vulnerable to RPL are at higher risk of ATH and women with a family history of ATH have a predisposition to have pregnancy loss. These data underline the existence of potential common biomarkers to these two pathologies. Thus, the aim of this study is to identify the biomarkers of RPL linked to ATH in order to understand the vascular molecular processes of RPL and to offer personalized therapy in the future. Methods: A human monoclonal antibody named P3, selected for its specificity against the galectin 3 protein (Gal3) over expressed in atheroma, was tested on human placental biopsies from RPL and compared with a control group of placentas obtained from normal childbirth. For the histological characterization of placental lesions, placental biopsies were stained with hematoxylin and eosin. The bio-reactivity of P3 was tested by immunohistochemistry and the staining was quantified using imageJ software. To identify P3 target in placental protein extracts, immunoprecipitations were performed and the eluates were analyzed by western blot followed by proteomics studies to validate gal3 as the placental P3 target. Results: highlight P3 bio-reactivity on placenta with a staining 3.8-fold higher in pathological placentas compared to controls. Conclusions: These results hold great promise for the choice of galectin 3 as biomarker for atherosis and the use of P3 antibody for the prevention and therapy of recurrent pregnancy losses