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Programming of stress pathways: A transgenerational perspective.

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Glucocorticoids (GC) are vital for fetal development and organ maturation. Prenatal GC exposure, including synthetic forms, can alter fetal epigenetic profiles, impacting stress responses and behavior across generations.

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Area of Science:

  • Developmental biology
  • Neuroendocrinology
  • Epigenetics

Background:

  • Glucocorticoids (GC) are critical developmental signals influencing fetal organ maturation, particularly the brain.
  • Fetal GC levels naturally surge late in gestation, impacting epigenetic profiles.
  • Premature GC surges due to stress or synthetic GC (sGC) exposure can have lasting effects.

Purpose of the Study:

  • To investigate the role of GC in fetal development and epigenetic programming.
  • To understand the consequences of altered GC exposure on fetal brain development and HPA axis function.
  • To examine the sex-specific and transgenerational inheritance of GC-induced epigenetic changes.

Main Methods:

  • Analysis of fetal epigenetic profiles in response to GC surge.
  • Investigation of GC-induced changes in gene transcription and HPA axis regulation.
  • Utilizing animal models to study effects of prenatal GC exposure on behavior and inheritance.

Main Results:

  • GC surge is associated with significant changes in fetal brain epigenetic profiles.
  • Prenatal GC overexposure leads to altered HPA axis function, stress responses, and mood disorders.
  • GC programming exhibits sex-specific effects and can be inherited across generations.

Conclusions:

  • GC exposure during gestation significantly impacts fetal development and epigenetic programming.
  • Altered GC levels can lead to long-term neurodevelopmental and behavioral consequences.
  • GC-induced epigenetic modifications can be transmitted across generations, highlighting the importance of managing prenatal GC exposure.