JCI online early table of contents: April 15, 2008

TITLE: ROCK1 mediates leukocyte recruitment and neointima formation following vascular injury

AUTHOR CONTACT:

James K. Liao
Brigham and Women’s Hospital and Harvard Medical School, Boston, Massachusetts, USA.
Phone: (617) 768-8424; Fax: (617) 768-8425; E-mail:

View the PDF of this article at: https://www.the-jci.org/article.php?id=29226

GASTROENTEROLOGY

‘Til death do us part: death of nerves in the gut causes intestinal disease

The nerves that control the gut form part of a network known as the enteric nervous system. Dysfunction in this system can lead to intestinal diseases such as Hirschsprung disease (also known as congenital intestinal aganglionosis), which occurs when part of the enteric nervous system is missing, meaning that the gut cannot function properly, leading to intestinal blockages and inflammation. Hirschsprung disease occurs most commonly in children born with mutations in their RET gene, but the reasons for this link have not been determined. In a new study, Hideki Enomoto and colleagues at the RIKEN Center for Developmental Biology in Kobe, Japan, have demonstrated that mice with reduced expression of the Ret gene show features of Hirschsprung disease. Disease was associated with impaired migration of precursors of enteric nerves to the gut and decreased survival of these precursor cells. If expression of the Ret gene was reduced after precursors of enteric nerves had migrated to the gut and developed into nerves, the enteric nerves that had already developed did not survive. Thus, the authors suggest that decreased Ret expression impairs the survival of both precursors of enteric nerves and enteric nerves themselves and that this cell death is potentially involved in the etiology of Hirschsprung disease.

TITLE: Diminished Ret expression compromises neuronal survival in the colon and causes intestinal aganglionosis in mice

AUTHOR CONTACT:

Hideki Enomoto
RIKEN Center for Developmental Biology, Kobe, Japan.
Phone: 81-78-306-3099, Fax: 81-78-306-3089, E-mail: .

View the PDF of this article at: https://www.the-jci.org/article.php?id=34425