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Yap is essential for uterine decidualization through Rrm2/GSH/ROS pathway in response to Bmp2

Hai-Fan Yu1,2, Zhan-Qing Yang1, Ming-Yue Xu1

  • 1College of Veterinary Medicine, Jilin University, Changchun, P. R. China.

International Journal of Biological Sciences
|April 13, 2022
PubMed

Insights

The YAP protein is crucial for uterine decidualization, regulating stromal cell proliferation and differentiation. Its pathway involves Bmp2, Rrm2, and the GSH/ROS balance, impacting DNA damage and mitochondrial function.

Area of Science:

  • Reproductive Biology
  • Cellular Biology
  • Molecular Endocrinology

Background:

  • YAP (Yes-associated protein) is vital for ovarian follicle and early embryo development.
  • Its specific role in decidualization, the process of preparing the uterus for pregnancy, remains largely unexplored.

Purpose of the Study:

  • To investigate the physiological significance of YAP in decidualization.
  • To elucidate the interplay between YAP, Bmp2, Rrm2, glutathione (GSH), and reactive oxygen species (ROS) in this process.

Main Methods:

  • Analysis of YAP expression in decidual cells.
  • Assessment of stromal cell proliferation, differentiation, and cell cycle progression upon YAP inactivation.
  • Investigation of the Bmp2/Alk2/YAP/Tead/Rrm2 signaling axis.
  • Measurement of intracellular ROS, GSH levels, and assessment of DNA damage.
  • Evaluation of mitochondrial function, including ATP levels, mtDNA copy number, and mitochondrial membrane potential.
  • Utilizing Mito-TEMPO as a mitochondrial antioxidant.

Main Results:

  • YAP is abundant in decidual cells; its inactivation impairs stromal cell proliferation, differentiation, and G1/S phase transition.
  • Bmp2 signaling promotes YAP nuclear translocation, which interacts with Tead to activate Rrm2, rescuing differentiation defects and attenuating DNA damage.
  • YAP inactivation leads to increased ROS, altered glutathione activity, and impaired mitochondrial function, which are counteracted by GSH replenishment.
  • Mitochondrial dysfunction, including increased apoptosis and altered ATP levels, is observed upon YAP blockage but is neutralized by GSH.
  • Mitochondrial antioxidant Mito-TEMPO rescues differentiation defects caused by YAP inactivation.

Conclusions:

  • YAP is essential for uterine decidualization.
  • YAP regulates decidualization via the Rrm2/GSH/ROS pathway in response to Bmp2 signaling.
  • YAP plays a critical role in maintaining mitochondrial function and preventing DNA damage during decidualization.
Keywords:
Bmp2Rrm2/GSH/ROS pathwayYapdecidualizationmitochondrial function

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