The potential contribution of stromal cell-derived factor 2 (SDF2) in endoplasmic reticulum stress response in severe preeclampsia and labor-onset

• Published in: Biochimica et biophysica acta. Molecular basis of disease 2020-02, Vol.1866 (2), p.165386-165386, Article 165386
• Main Authors: Lorenzon-Ojea, Aline R., Yung, Hong Wa, Burton, Graham J., Bevilacqua, Estela
• Format: Article
• Language: English
• Subjects: Labor; Placenta; Preeclampsia; SDF2; Trophoblast; UPR
• ISSN: 0925-4439; 1879-260X
• DOI: 10.1016/j.bbadis.2019.01.012

Endoplasmic reticulum (ER) stress occurs when the protein folding machinery in the cell is unable to cope with newly synthesized proteins, which results in an accumulation of misfolded proteins in the ER lumen. In response, the cell activates a cellular signaling pathway known as the Unfolded Protein Response (UPR), aiming to restore cellular homeostasis. Activation and exacerbation of the UPR have been described in several human pathologies, including cancer and neurological disorders, and in some gestational diseases such as preeclampsia and gestational diabetes. This review explores the participation of stromal cell-derived factor 2 (SDF2) in UPR pathways, shows new information and discusses its exacerbation regarding protein expression in severe preeclampsia and labor, both of which are associated with ER stress. •Evidence from other studies shows that SDF2 is part of the family of proteins involved in the activation of ER stress/UPR.•Experimental approaches suggest SDF2 is associated with the balance of cell death/cell survival program mediated by PERK arm of UPR.•SDF2 increased levels in placentas from sPE and labor may contribute to placental impairment and gestational diseases.