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[MTHFR gene silencing affects mouse embryonic palatal mesenchymal cell proliferation and apoptosis]

Wen-lin Xiao1, Bing Shi, Qian Zheng

  • 1Department of Oral and Maxillofacial Surgery, Medical School of Qingdao University, Qingdao 266003, Shandong Province, China. wenlinxiao@sina.com.cn

Shanghai Kou Qiang Yi Xue = Shanghai Journal of Stomatology
|August 4, 2009
PubMed
Abstract

Insights

Methylenetetrahydrofolate reductase (MTHFR) gene silencing reduces embryonic palatal mesenchymal cell proliferation and increases apoptosis. This suggests a role for MTHFR gene variants in non-syndromic cleft lip and palate development.

Area of Science:

  • Genetics
  • Developmental Biology
  • Cell Biology

Background:

  • Non-syndromic cleft lip and palate (NCLP) is a common birth defect with complex etiology.
  • Genetic factors, including mutations in the methylenetetrahydrofolate reductase (MTHFR) gene, are implicated in NCLP pathogenesis.
  • MTHFR plays a crucial role in folate metabolism, essential for DNA synthesis and repair during embryonic development.

Purpose of the Study:

  • To investigate the role of MTHFR gene variants in the pathogenesis of NCLP.
  • To examine the effect of MTHFR gene silencing on mouse embryonic palatal mesenchymal (EPM) cell proliferation and apoptosis.

Main Methods:

  • RNA interference (RNAi) was used to silence the MTHFR gene in primary EPM cell cultures.
  • MTHFR shRNA expression vectors were constructed for gene silencing.
  • Cell proliferation was assessed using MTT assays.
  • Apoptosis was measured by flow cytometry (FCM).
  • Statistical analysis was performed using SPSS, with ANOVA for proliferation and U-test for apoptosis.

Main Results:

  • MTHFR gene silencing significantly reduced EPM cell proliferation compared to control groups (P<0.001).
  • A significant increase in apoptotic cell number was observed following MTHFR gene silencing (P<0.05).
  • Silenced cells exhibited slower growth rates.

Conclusions:

  • MTHFR gene silencing negatively impacts EPM cell proliferation and induces apoptosis.
  • These findings suggest that MTHFR gene variants and associated metabolic dysfunction may contribute to the pathological basis of NCLP.
  • The results highlight the importance of MTHFR in palate development and its potential link to NCLP, especially under conditions of insufficient folic acid supplementation.

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