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New Study Suggests the Fetus is Responsible For Initiating Labor

Last updated June 27, 2015

Approved by: Krish Tangella MD, MBA, FCAP

"By understanding the factors and pathways that initiate normal-term labor at 40 weeks, we can gain more insight into how to prevent preterm labor," according to Dr. Mendelson, the Director of the North Texas March of Dimes Birth Defects Center at UT Southwestern Medical Center.


Researchers at the UT Southwestern Medical Center have identified proteins located in a fetus’ lungs that are responsible for initiating the birthing process in the mother, offering prospective new targets for averting preterm birth.

There have been several previous studies that suggested the fetus is responsible for initiating the labor process, but the exact mechanisms involved remained uncertain. The findings from this study are the first to pinpoint the exact cause of the initiation of labor.

 The study utilized mouse models, which found that two proteins, steroid receptor coactivators 1 and 2 (SRC-1 and SRC-2), regulate genes for lung surfactant components that stimulate labor. Lung surfactant is a substance released from the lungs of the fetus prior to birth that helps initiate normal breathing outside of the womb. The release of these proteins, along with surfactant protein A (SP-A) and platelet-activating factor (PAF), which are up-regulated in response to the release of SRC-1 and SRC-2, initiate an inflammatory response in the uterus of the mother, which stimulates the labor process.

 The study, published in the Journal of Clinical Investigation,exhibited that a deficiency in SRC-1 and SRC-2 in the lungs of the fetus dramatically decrease the production of SP-A and PAF, which in turn delays the labor process in a mouse model by one to two days. This time delay is analogous to a three to four week delay in labor for women.

With the understanding of these vital proteins, the researchers found that injecting SP-A and PAF into the amniotic fluid in mice that were deficient in these substances allowed the mouse mothers to deliver on time.

"By understanding the factors and pathways that initiate normal-term labor at 40 weeks, we can gain more insight into how to prevent preterm labor," according to Dr. Mendelson, the Director of the North Texas March of Dimes Birth Defects Center at UT Southwestern Medical Center.

According to the Centers for Disease Control and Prevention, one in every nine children are born premature in the United States, and the study proclaims that 1.1 million children die globally each year due to premature birth. These statistics, correlated with the significance of these findings, suggest a step in the right direction towards protecting the future generations of children born around the world.

Additional research is necessary to define the mechanisms in which the fetal signals are transmitted to the mother’s uterus and connecting these discoveries to the triggers of preterm labor.

By Melissa Pillote

Primary Reference:

Gao, L., Rabbitt, E.H., Condon, J.C., Renthal, N.E., Johnston, J.M., Mitsche, M.A., Chambon, P., Xu, J., O’Malley, B.W., & Mendelson, C.R. (2015). Steroid receptor coactivators 1 and 2 mediate fetal-to-maternal signaling that initiates parturition. The Journal of Clinical Investigation.Retrieved from http://www.jci.org/articles/view/78544

Additional References:

 Preterm Birth. Retrieved from http://www.cdc.gov/reproductivehealth/maternalinfanthealth/pretermbirth.htm

Reviewed and Approved by a member of the DoveMed Editorial Board
First uploaded: June 27, 2015
Last updated: June 27, 2015