Related Experiment Video
Updated: May 28, 2026
09:04
Generation of Self-assembled Vascularized Human Skin Equivalents
Published on: February 12, 2021
Vitamin A and clefting: putative biological mechanisms
Mignon M G Ackermans1, Huiqing Zhou, Carine E L Carels
1Department of Orthodontics and Craniofacial Biology, Nijmegen Centre for Molecular Life Sciences, Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands.
Nutrition Reviews
|October 5, 2011
Summary
Maternal vitamin A intake impacts embryonic development, potentially causing cleft palate. Understanding how excess vitamin A affects palatogenesis is crucial for developing preventive nutritional strategies.
Area of Science:
- Developmental Biology
- Nutritional Science
- Teratology
Background:
- Nutritional factors, including vitamin intake, are implicated in the development of cleft palate.
- Vitamin A plays a critical role in embryonic development and is known to cause congenital malformations when in excess.
Purpose of the Study:
- To review the biological mechanisms linking maternal vitamin A intake to cleft palate.
- To identify how excessive vitamin A may disrupt the stages of palatogenesis.
Main Methods:
- Literature review of studies investigating vitamin A and palatogenesis.
- Analysis of proposed biological pathways affected by vitamin A during embryonic development.
Main Results:
- Excess vitamin A can interfere with cell proliferation, extracellular matrix composition, and epithelial differentiation/apoptosis during palatogenesis.
- High doses of vitamin A impact palatogenesis by affecting cell proliferation and growth factors like TGF-β and PDGF.
Conclusions:
- Excessive maternal vitamin A intake poses a risk for cleft palate development through multiple mechanisms during palatogenesis.
- Further research into the effects of lower vitamin A doses is needed to refine public health recommendations for preventing cleft palate.
Related Concept Videos
01:29Tight Junctions
Tight junctions are molecular seals between cells that prevent the leaking of fluids, ions, and other small solutes across cavities and compartments in multicellular organisms. They are mainly composed of claudin and occludin transmembrane proteins, and other proteins such as tricellulin and JAM (junctional adhesion molecule). All these proteins are 4-pass transmembrane proteins, except JAM, which is a single-pass transmembrane protein belonging to the immunoglobulin superfamily. The...
01:24Regulation of Angiogenesis and Blood Supply
Rapidly dividing tumors, embryos, and wounded tissues require more oxygen than usual, lowering the oxygen concentration in the blood. At low oxygen or hypoxic conditions, an oxygen-sensitive transcription factor called the hypoxia-inducible factor 1 or HIF1 is activated. HIF1 is a dimeric protein of alpha (ɑ) and beta (β) subunits. Under optimal oxygen conditions, HIF1β is present in the nucleus while HIF1ɑ remains in the cytosol. HIF1ɑ is hydroxylated by prolyl hydroxylase and factor...
01:25Structure of Cadherins
The cadherins were one of the first cell adhesion molecules discovered; the term “cadherins” is based on their calcium-dependent adhering properties. The first cadherins discovered on the epithelial, neuronal, and placental cells were named E-cadherin, P-cadherin, and N-cadherin, respectively. These classical cadherins share sequence and structural similarities. Other cadherins, including those involved in cell signaling, are grouped into non-classical cadherins. This diversity of cadherins...
01:23Cystic Fibrosis: Pathogenesis
Cystic fibrosis (CF), an autosomal recessive disorder, significantly affects the function of exocrine glands. This genetically inherited disease is characterized by the production of thick and sticky mucus, which can severely affect various organs and systems in the body.
CF is primarily caused by a genetic mutation in a chromosome 7 gene coding for the cystic fibrosis transmembrane conductance regulator (CFTR) protein. The most common gene mutation leading to CF is the ΔF508 mutation, but...
CF is primarily caused by a genetic mutation in a chromosome 7 gene coding for the cystic fibrosis transmembrane conductance regulator (CFTR) protein. The most common gene mutation leading to CF is the ΔF508 mutation, but...
01:13Cell-matrix's Response to Mechanical Forces
In animal cells, the extracellular matrix allows cells within tissues to withstand external stresses and transmits signals from the outside of the cell to the inside. The extracellular matrix is extensive, and its composition varies between different types of tissues. For example, the reticular fibers and ground substance make up the ECM in loose connective tissue, while collagen and bone minerals make up the ECM of bone tissue.
Anchoring junctions mechanically attach a cell to the...
Anchoring junctions mechanically attach a cell to the...
01:15Mechanisms of Membrane-bending
The living membranes are flexible due to their fluid mosaic nature; however, their bending into different shapes is an active process regulated by specific lipids and proteins. The membrane bending can be transient as seen in vesicles or stable for a long time as in microvilli. Cells regulate the size, location, and duration of the membrane curvature.
Membrane bending can happen due to intrinsic changes in lipid composition or extrinsic association with different proteins. The proteins involved...
Membrane bending can happen due to intrinsic changes in lipid composition or extrinsic association with different proteins. The proteins involved...