MYC-induced nuclear antigen (MINA) and preeclampsia

Martínez‐Fierro, Margarita L.; Reyes-Oliva, Edwin A; Cabral-Pacheco, Griselda A.; Garza‐Veloz, Idalia; Aceves-Medina, Maria C.; Luevano, Martha; Barbosa-Cisneros, O; Galván-Valencia, Marisol; Yahuaca-Mendoza, Patricia; Delgado‐Enciso, Iván; Zamudio-Osuna, Michelle; Rodríguez‐Sánchez, Iram P.; Vázquez-Castro, Rosbel; Guerrero-Saucedo, Marycruz

doi:10.3109/10641955.2015.1130833

Cited by 1 publication

(1 citation statement)

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“…While genome-wide analyses have identified genes deregulated in PE, only a few transcription factors (TFs) have been shown to be associated with normal TE specification and/or human placental differentiation (Hemberger et al, 2010; Martinez-Fierro et al, 2016). Its strong similarity with human placentation makes the mouse an excellent model to elucidate key mechanisms of placental development.…”

Section: Introductionmentioning

confidence: 99%

ARID3A is required for mammalian placenta development

Rhee

Edwards

Dang

et al. 2017

Developmental Biology

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Previous studies in the mouse indicated that ARID3A plays a critical role in the first cell fate decision required for generation of trophectoderm (TE). Here, we demonstrate that ARID3A is widely expressed during mouse and human placentation and essential for early embryonic viability. ARID3A localizes to trophoblast giant cells and other trophoblast-derived cell subtypes in the junctional and labyrinth zones of the placenta. Conventional Arid3a knockout embryos suffer restricted intrauterine growth with severe defects in placental structural organization. Arid3a null placentas show aberrant expression of subtype-specific markers as well as significant alteration in cytokines, chemokines and inflammatory response-related genes, including previously established markers of human placentation disorders. BMP4-mediated induction of trophoblast stem (TS)-like cells from human induced pluripotent stem cells results in ARID3A up-regulation and cytoplasmic to nuclear translocation. Overexpression of ARID3A in BMP4-mediated TS-like cells up-regulates TE markers, whereas pluripotency markers are down-regulated. Our results reveal an essential, conserved function for ARID3A in mammalian placental development through regulation of both intrinsic and extrinsic developmental programs.

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Section: Introductionmentioning

confidence: 99%