Genomics

Dataset Information

0

PM2.5 leads to adverse pregnancy outcomes by inducing trophoblast oxidative stress and mitochondrial apoptosis via KLF9/CYP1A1 transcriptional axis


ABSTRACT: Epidemiological studies have demonstrated that fine particulate matter (PM2.5) is associated with adverse obstetric and postnatal metabolic health outcomes, but the mechanism remains unclear. This study aimed to investigate the toxicological pathways by which PM2.5 damaged placental trophoblasts in vivo and in vitro. We confirmed that PM2.5 induced adverse gestational outcomes such as increased fetal mortality rates, decreased fetal number and weight, damaged placental structure, and increased apoptosis of trophoblasts. Additionally, PM2.5 induced dysfunction of the trophoblast cell line HTR8/SVneo, including in its proliferation, apoptosis, invasion, migration and angiogenesis. Moreover, we comprehensively analyzed the transcriptional landscape of HTR8/SVneo cells exposed to PM2.5 through RNA-Seq and observed that PM2.5 triggered overexpression of pathways involved in oxidative stress and mitochondrial apoptosis to damage HTR8/SVneo cell biological functions through CYP1A1. Mechanistically, PM2.5 stimulated KLF9, a transcription factor identified as binding to CYP1A1 promoter region, which further modulated the CYP1A1-driven downstream phenotypes. Together, this study demonstrated that the KLF9/CYP1A1 axis played a crucial role in the toxic progression of PM2.5 induced adverse pregnancy outcomes, suggesting adverse effects of environmental pollution on pregnant females and putative targeted therapeutic strategies.

ORGANISM(S): Homo sapiens

PROVIDER: GSE237795 | GEO | 2023/08/01

REPOSITORIES: GEO

Similar Datasets

2021-08-27 | GSE182717 | GEO
2018-07-05 | PXD005045 | Pride
2018-01-30 | GSE105783 | GEO
2021-06-08 | PXD026574 | iProX
2020-12-01 | GSE148962 | GEO
2021-08-05 | GSE155750 | GEO
2022-08-14 | GSE211010 | GEO
2023-04-30 | GSE183072 | GEO
2014-12-31 | GSE50945 | GEO
2021-12-16 | GSE189187 | GEO