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Nitric oxide regulates blastocyst hatching in mice.

Xiaoyan Pan1, Xuenan Wang2, Xiyan Wang1

  • 1Department of Histology and Embryology, Jilin Medical University Jilin 132013, P. R. China.

International Journal of Clinical and Experimental Medicine
|July 30, 2015
PubMed
Summary

Nitric oxide (NO) regulates mouse blastocyst hatching via the NO/cGMP pathway. Both too much and too little NO disrupt hatching, with excess NO inducing apoptosis in blastocyst cells.

Keywords:
MouseNO/cGMP pathwayapoptosisblastocyst hatchingnitric oxide

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Area of Science:

  • Reproductive biology
  • Developmental biology
  • Cell signaling

Background:

  • Blastocyst hatching is a critical step in mammalian reproduction.
  • Nitric oxide (NO) is a signaling molecule with diverse physiological roles.
  • The role of NO in blastocyst hatching requires further elucidation.

Purpose of the Study:

  • To investigate the regulatory role of nitric oxide (NO) in mouse blastocyst hatching.
  • To examine the involvement of the NO/cGMP pathway in this process.

Main Methods:

  • Mouse morulae were cultured in vitro with varying concentrations of L-NAME (NO synthase inhibitor), SNP (NO donor), and 8-Br-cGMP (cGMP analog).
  • Blastocyst hatching rates were assessed.
  • Expression of epithelial nitric oxide synthase (eNOS) and active caspase-3 was analyzed using confocal microscopy.

Main Results:

  • L-NAME reduced eNOS expression, while increasing L-NAME, SNP, or 8-Br-cGMP concentrations inhibited blastocyst hatching.
  • Low concentrations of SNP or 8-Br-cGMP reversed L-NAME-induced hatching inhibition.
  • SNP elevated active caspase-3 expression, indicating apoptosis, whereas L-NAME and 8-Br-cGMP did not significantly affect it.

Conclusions:

  • The NO/cGMP pathway is crucial for successful mouse blastocyst hatching.
  • Both NO deficiency and excess NO negatively impact blastocyst hatching.
  • Excessive NO can induce apoptosis in blastocyst cells, hindering hatching.