Science News

... from universities, journals, and other research organizations

Scientists Uncover A New Mechanism Regulating Fetal Growth And Neonatal Survival

Sep. 21, 2009 — Dr. Sylvain Meloche, Principal Investigator at the Institute for Research in Immunology and Cancer (IRIC) of the Université de Montréal, and his colleagues have uncovered the critical role played by the protein kinase Erk3 in fetal growth potential and lung maturation. The recent findings, published in the online early edition of the Proceedings of the National Academy of Sciences, reveal that the loss of Erk3 function in the mouse leads to fetal growth restriction and early neonatal lethality caused by respiratory distress.


Share This:

Respiratory distress syndrome is a serious complication of premature and intrauterine growth-restricted infants and represents the primary contributor to neonatal morbidity and mortality. Intrauterine growth restriction (IUGR) refers to a condition in which the fetus fails to achieve its genetically determined size and is consequently smaller than expected for its gestational age. It results from defects that prevent the multiplication or growth of cells, leading to a decrease in organ size and function. To date, only few molecular mechanisms have been proposed to explain this complex condition. In this study, Dr. Meloche and his team demonstrate that the inactivation of Erk3 in mice mimics IUGR conditions in humans and is associated with decreased blood levels of IGF-2, a growth hormone promoting fetal development.

"Infants with IUGR have a significant risk for diabetes, hypertension and coronary heart disease later in life," explains Dr. Meloche, "IUGR is also associated with a higher risk of long-term neurodevelopmental outcomes. We hope that this study will shed new light on the molecular mechanisms underlying this serious condition."

Dr. Meloche and his team intend to exploit this new mouse model to further the understanding of the genetic and biochemical pathways involved in fetal growth control and pulmonary maturation.

Share this story on Facebook, Twitter, and Google:

Other social bookmarking and sharing tools:

|

Story Source:

The above story is reprinted from materials provided by University of Montreal.

Note: Materials may be edited for content and length. For further information, please contact the source cited above.


Journal Reference:

  1. Klinger et al. Loss of Erk3 function in mice leads to intrauterine growth restriction, pulmonary immaturity, and neonatal lethality. Proceedings of the National Academy of Sciences, 2009; DOI: 10.1073/pnas.0900919106
APA

MLA

Note: If no author is given, the source is cited instead.

Search ScienceDaily

Number of stories in archives: 137,427

Find with keyword(s):
 
Enter a keyword or phrase to search ScienceDaily's archives for related news topics,
the latest news stories, reference articles, science videos, images, and books.

Recommend ScienceDaily on Facebook, Twitter, and Google:

Other social bookmarking and sharing services:

|

 
  more breaking science news

Social Networks


Follow ScienceDaily on Facebook, Twitter,
and Google:

Recommend ScienceDaily on Facebook, Twitter, and Google +1:

Other social bookmarking and sharing tools:

|

Breaking News

... from NewsDaily.com

In Other News ...

Science Video News


Helping Cancer Survivors Grow Up

Studying childhood cancer patients who have suffered tissue and organ damage from chemotherapy treatments, researchers have found that growth. ...  > full story

Strange Science News

 

Free Subscriptions

... from ScienceDaily

Get the latest science news with our free email newsletters, updated daily and weekly. Or view hourly updated newsfeeds in your RSS reader:

Feedback

... we want to hear from you!

Tell us what you think of ScienceDaily -- we welcome both positive and negative comments. Have any problems using the site? Questions?

Post this page to your favorite social bookmarking site:
Include this item in your blog or web site:
Cite this article in your essay, paper, or report:
Email this page's link to a friend or colleague: