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Related Concept Videos

Teratogenicity01:07

Teratogenicity

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The ability of a drug to produce structural deformations and functional abnormalities in the developing embryo or the fetus is called teratogenicity, and the drug producing this effect is known as a teratogen. Teratogenic effects include stillbirth, miscarriage, intrauterine growth restriction, and neurocognitive delay. A teratogen may affect the embryo at different stages of development, which is important in determining the type and extent of the damage. During blastocyst formation, the early...
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Using Chicken Embryo as a Powerful Tool in Assessment of Developmental Cardiotoxicities
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Magnesium and embryonic development.

Yuko Komiya1, Li-Ting Su2, Hsiang-Chin Chen3

  • 1Department of Pharmacology, Rutgers Robert Wood Johnson Medical School, 675 Hoes Lane, Piscataway, NJ 08854, USA.

Magnesium Research
|April 12, 2014
PubMed
Summary
This summary is machine-generated.

Magnesium (Mg2+) is crucial for embryonic development, particularly in gastrulation and neural tube closure. Supplementing magnesium can prevent developmental defects linked to TRPM7 ion channel function.

Keywords:
TRPM6TRPM7gastrulationion channelkinasemagnesium

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Area of Science:

  • Developmental Biology
  • Molecular Biology
  • Cellular Physiology

Background:

  • Magnesium (Mg2+) is vital for adult cellular functions but its role in early embryonic development is less understood.
  • Gestational Mg2+ deficiency causes teratogenic effects in rodents and is linked to human birth defects like spina bifida.
  • TRPM7 and TRPM6 ion channels, involved in Mg2+ homeostasis, are potential regulators of early development.

Purpose of the Study:

  • To review molecular, biochemical, and electrophysiological data on TRPM6 and TRPM7.
  • To elucidate the role of Mg2+ in early embryonic development via these unique channel-kinases.
  • To present a model for Mg2+ impact on gastrulation and neural fold closure.

Main Methods:

  • Review of molecular genetic studies on TRPM6 and TRPM7.
  • Analysis of biochemical and electrophysiological data.
  • Examination of studies involving TRPM7/TRPM6 disruption in model organisms.

Main Results:

  • TRPM7 and TRPM6 are essential for Mg2+ homeostasis and vertebrate development.
  • Disruption of TRPM7/TRPM6 function in model organisms impairs gastrulation and neural tube closure.
  • Mg2+ supplementation prevents gastrulation defects caused by TRPM7 depletion.

Conclusions:

  • Mg2+ plays a critical, specific role in early embryonic development, particularly gastrulation and neural fold closure.
  • TRPM7 and TRPM6 channel-kinases are key mediators of Mg2+'s developmental functions.
  • Understanding Mg2+ regulation through TRPM7/TRPM6 offers insights into preventing birth defects.