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Air pollution-linked epigenetic modifications in placental DNA: Prognostic potential for identifying future foetal anomalies.
Kumar, Sruthy Hari; Acharyya, Sayanti; Chouksey, Apoorva; Soni, Nikita; Nazeer, Nazim; Mishra, Pradyumna Kumar.
Afiliación
  • Kumar SH; Division of Environmental Biotechnology, Genetics & Molecular Biology (EBGMB), ICMR-National Institute for Research in Environmental Health (NIREH), Bhopal, India.
  • Acharyya S; Division of Environmental Biotechnology, Genetics & Molecular Biology (EBGMB), ICMR-National Institute for Research in Environmental Health (NIREH), Bhopal, India.
  • Chouksey A; Division of Environmental Biotechnology, Genetics & Molecular Biology (EBGMB), ICMR-National Institute for Research in Environmental Health (NIREH), Bhopal, India.
  • Soni N; Division of Environmental Biotechnology, Genetics & Molecular Biology (EBGMB), ICMR-National Institute for Research in Environmental Health (NIREH), Bhopal, India.
  • Nazeer N; Division of Environmental Biotechnology, Genetics & Molecular Biology (EBGMB), ICMR-National Institute for Research in Environmental Health (NIREH), Bhopal, India.
  • Mishra PK; Division of Environmental Biotechnology, Genetics & Molecular Biology (EBGMB), ICMR-National Institute for Research in Environmental Health (NIREH), Bhopal, India. Electronic address: pkm_8bh@yahoo.co.uk.
Reprod Toxicol ; 129: 108675, 2024 Oct.
Article en En | MEDLINE | ID: mdl-39074641
ABSTRACT
Prenatal exposure to air pollution is a significant risk factor for the mother and the developing foetus. The accumulation of pollutants in the placenta can cause a self-cascade loop of pro-inflammatory cytokine responses and DNA double-strand breaks. Previous research has shown that airborne particulate matter can damage the epigenome and disturb mitochondrial machinery, ultimately impairing placental function. Mitochondria are essential for preserving cellular homeostasis, energy metabolism, redox equilibrium, and epigenetic reprogramming. As these organelles are subtle targets of environmental exposures, any disruption in the signaling pathways can result in epigenomic instability, which can impact gene expression and mitochondrial function. This, in turn, can lead to changes in DNA methylation, post-translational histone modifications, and aberrant expression of microRNAs in proliferating trophoblast cells. The placenta has two distinct layers, cytotrophoblasts, and syncytiotrophoblasts, each with its mitochondria, which play important roles in preeclampsia, gestational diabetes, and overall health. Foetal nucleic acids enter maternal circulation during placental development because of necrotic, apoptotic, and inflammatory mechanisms. These nucleic acids reflect normal or abnormal ongoing cellular changes during prenatal foetal development. Detecting cell-free DNA in the bloodstream can be a biomarker for predicting negative pregnancy-related outcomes and recognizing abnormalities in foetal growth. Hence, a thorough understanding of how air pollution induces epigenetic variations within the placenta could offer crucial insights into underlying mechanisms and prolonged repercussions on foetal development and susceptibility in later stages of life.
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Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Placenta / Epigénesis Genética Límite: Animals / Female / Humans / Pregnancy Idioma: En Revista: Reprod Toxicol Asunto de la revista: EMBRIOLOGIA / MEDICINA REPRODUTIVA / TOXICOLOGIA Año: 2024 Tipo del documento: Article Pais de publicación: Estados Unidos

Texto completo: 1 Colección: 01-internacional Base de datos: MEDLINE Asunto principal: Placenta / Epigénesis Genética Límite: Animals / Female / Humans / Pregnancy Idioma: En Revista: Reprod Toxicol Asunto de la revista: EMBRIOLOGIA / MEDICINA REPRODUTIVA / TOXICOLOGIA Año: 2024 Tipo del documento: Article Pais de publicación: Estados Unidos