Spatiotemporal expression of leukemia inhibitory factor receptor protein during neural tube development in embryos with neural tube defects

Neural Regen Res, 2020 · DOI: 10.4103/1673-5374.266921 · Published: October 18, 2019

Simple Explanation

Neural tube defects (NTDs) are severe congenital malformations affecting the central nervous system. This study explores the role of Leukemia Inhibitory Factor Receptor (LIFR) in the development of NTDs. The study used a rat model of spina bifida aperta (SBA) induced by retinoic acid to examine the spatiotemporal expression of LIFR during fetal development. The research found that LIFR expression is significantly downregulated in the spinal cords of rats with SBA compared to healthy rats, suggesting a potential role of LIFR in the pathogenesis of NTDs.

Study Duration

Embryonic day 11 to 17

Participants

Seventy-eight specific-pathogen-free female Wistar rats and human fetal samples (10 NTD, 10 control)

Evidence Level

Not specified

Key Findings

1
LIFR protein and mRNA expression in the spinal cords of normal rat embryos increased with embryonic development from E11 to E17.
2
LIFR was significantly downregulated in the spinal cords of spina bifida aperta rats compared with healthy rats from embryonic days 11 to 17.
3
LIFR mRNA expression was significantly down-regulated in spinal cords of human fetuses with neural tube defects compared with normal controls at a gestational age of 24 to 33 weeks.

Research Summary

This study investigates the spatiotemporal expression of LIFR in normal and neural tube defect (NTD) embryos to understand its role in NTD pathogenesis. A rat model of spina bifida aperta (SBA) was used, and LIFR expression was examined via real-time PCR, western blot, and immunohistochemistry. The results showed that LIFR expression increases during normal embryonic development but is significantly downregulated in SBA rats compared to healthy controls. Similar downregulation was observed in human NTD fetuses. The study concludes that LIFR plays a specific role in neural tube development, and its downregulation may contribute to the pathogenesis of NTDs. These findings provide insights into LIFR's role and may facilitate the development of therapeutic interventions.

Practical Implications

Understanding NTD Pathogenesis

The study's findings provide a deeper understanding of the molecular mechanisms underlying neural tube defects, specifically highlighting the role of LIFR.

Potential Therapeutic Target

LIFR's involvement in neural tube development suggests that it could be a potential therapeutic target for preventing or treating NTDs.

Diagnostic Biomarker

The altered expression of LIFR in NTD embryos and fetuses could potentially be explored as a diagnostic biomarker for early detection of NTDs.

Study Limitations

1
The study primarily relies on an animal model of spina bifida, which may not fully replicate the complexity of human NTDs.
2
The sample size for human fetal samples was relatively small (n=10 per group), which might limit the generalizability of the findings.
3
Further research is needed to elucidate the specific LIFR signaling pathways and interaction partners involved in neural tube development.

Your Feedback

Was this summary helpful?

Back to Neurology