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Updated: May 25, 2025

Isolation and Time-Lapse Imaging of Primary Mouse Embryonic Palatal Mesenchyme Cells to Analyze Collective Movement Attributes
Published on: February 13, 2021
Glycolysis regulates palatal mesenchyme proliferation through Pten-Glut1 axis via Pten classical and non-classical
Yijia Wang1,2, Xia Peng1, Xiaotong Wang1
1Laboratory of Orofacial Development, Laboratory of Molecular Signaling and Stem Cells Therapy, Molecular Laboratory for Gene Therapy and Tooth Regeneration, Beijing Key Laboratory of Tooth Regeneration and Function Reconstruction, Capital Medical University School of Stomatology, No.9 Fanjiacun Road, Beijing, 100070, China.
Insights
Cleft palate (CP) lacks early treatment. Blocking phosphatase and tensin homolog (Pten) may prevent CP by targeting glycolysis during embryonic development, offering a novel therapeutic approach.
Area of Science:
- Developmental biology
- Molecular biology
- Biochemistry
Background:
- Cleft palate (CP) results from abnormal embryonic development and currently lacks interceptive treatments.
- Germline deletion of phosphatase and tensin homolog (Pten) is linked to embryonic malformations and influences glycolysis.
- The specific roles of Pten in CP and its connection to glycolysis remain largely unexplored.
Purpose of the Study:
- To investigate the role of Pten in cleft palate (CP) development.
- To explore the relationship between CP, Pten, and glycolysis.
- To assess the potential of Pten inhibition as an early interceptive treatment for CP.
Main Methods:
- Development of in vitro and in vivo Pten knockdown models.
- Utilizing Pten inhibitors, such as VO-OHpic, for experimental treatment.
- Analysis of the interplay between Pten, glycolysis, and palate development.
Main Results:
- Pten knockdown models were successfully constructed.
- Preliminary evidence suggests Pten inhibition may reduce CP occurrence.
- The study identified a crosstalk between Pten and glycolysis in palate development.
Conclusions:
- Blocking Pten presents a potential early interceptive strategy for preventing cleft palate.
- Intervention during early palate development, particularly when exposed to harmful environments, may be effective.
- The findings highlight the crucial role of the Pten-glycolysis pathway in embryonic palate formation.
Abstract:
Abnormal embryonic development leads to the formation of cleft palate (CP) which is difficult to be detected by genetic screening and needs sequent treatment from infants to adults. There are no interceptive treatment about CP until now. Germline deletion of phosphatase and tensin homolog (Pten) was related to embryonic malformation and regulated tumor cell proliferation through glycolysis. However, the role of Pten in CP and the relationship between CP, Pten, and glycolysis are unknown. In our research, we constructed Pten knockdown models in vitro and in vivo. Our results provided preliminary evidence that blocking Pten by its inhibitor such as VO-OHpic might be an effective interceptive treatment in early period of palate development when pregnant mother expose in harmful environment during the early period of palate development to reducing CP occurring which was related with the crosstalk between Pten, and glycolysis in the process.
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