Vitamin A Deficiency and Hirschsprung Disease

Dr. Robert Heuckeroth and his team and Washington University recently published more results on the link between maternal Vitamin A Deficiency and Hirschsprung Disease. It underscores the importance of maternal vitamin A nutrition for preventing the diease penetrance and expressitivity:
Ming Fu, Yoshiharu Sato, Ariel Lyons-Warren, Bin Zhang, Maureen A. Kane, Joseph L. Napoli and Robert O. Heuckeroth. Vitamin A facilitates enteric nervous system precursor migration by reducing Pten accumulation. Development 137, 631-640 (2010) doi:10.1242/dev.040550.
SUMMARY

Hirschsprung disease is a serious disorder of enteric nervous system (ENS) development caused by the failure of ENS precursor migration into the distal bowel. We now demonstrate that retinoic acid (RA) is crucial for GDNF-induced ENS precursor migration, cell polarization and lamellipodia formation, and that vitamin A depletion causes distal bowel aganglionosis in serum retinolbinding-protein-deficient (Rbp4–/–) mice. Ret heterozygosity increases the incidence and severity of distal bowel aganglionosis induced by vitamin A deficiency in Rbp4–/– animals. Furthermore, RA reduces phosphatase and tensin homolog (Pten) accumulation in migrating cells, whereas Pten overexpression slows ENS precursor migration. Collectively, these data support the hypothesis that vitamin A deficiency is a non-genetic risk factor that increases Hirschsprung disease penetrance and expressivity, suggesting that some cases of Hirschsprung disease might be preventable by optimizing maternal nutrition.

By the way, the lab has been an ongoing consumer of our Ret Antibody and referenced use of this antibody in the publication.

Image: E12.5 mouse mid-gut slices were cultured to allow crest-derived cells to migrate onto the dish in response to GDNF. Cultures were maintained for 16 hours without added retinoic acid.

Related Reagents:

Ret (C-Terminus Fused)
Ret-Fluorescein Labeled
Ret-Allophycocyanin Labeled
Ret-Phycoerythrin Labeled
Neurotrophins and Growth Factor Antibodies
Neurotrophins-Neuron/Glial Marker
Recombinant Proteins
Neuron/Glial Markers
Stem Cell Research Reagents

Stems Cells and SCI

This is fascinating and encouraging to sufferers of Spinal Cord Injury:

ScienceDaily (Oct. 9, 2010) — Researchers at Karolinska Institutet have shown how stem cells, together with other cells, repair damaged tissue in the mouse spinal cord. The results are of potential significance to the development of therapies for spinal cord injury: http://www.sciencedaily.com/releases/2010/10/101008082736.htm#

Enhancing Neurite Outgrowth

We are pleased to announce the addition of new proteins to our Axon Growth and Guidance category. These are designed to enhance neurite out growth.

Name	Catalog #	Type	Species	Size	Price
NGF-b, NSO Derived	PR15083	Protein	H; M; R	100 ug	$285
NGF-b, NSO Derived, CF	PR15084CF	Protein	H; M; R	100 ug	$285
S100A13, CF	PR15085CF-50	Protein	H; R	50 ug	$315
Slit1	PR15075-50	Protein	Ch; H	50 ug	$315
Slit2, CHO	PR15085-50	Protein	Ch; H	50 ug	$315

Image: Cultured chick dorsal root ganglion neurons were grown in the presence of recombinant human NGF-b with (A) or without (B) recombinant mouse Slit2. The presence of the Slit2 protein signifi cantly enhanced neurite outgrowth.