New gene linked to preeclampsia discovered

New gene linked to preeclampsia discovered
21 February 2011

Appeared in BioNews 596

A gene important in autoimmune disease has been linked to preeclampsia, a serious complication of pregnancy. The study from scientists at North Carolina State University looked at the genes that are switched on and off in the human placenta, to find genes that are differently expressed in preeclampsia.

The researchers found that, in placentas from women who had preeclampsia, a gene called sialic acid acetylesterase (SIAE) produces more than the normal amount of sialic acid acetylesterase protein. Mutations in the same gene have previously been linked to autoimmune disease. SIAE is thought to help regulate the activity of the immune system.

The researchers also linked a number of other genes involved with the immune system to preeclampsia, as well as confirming the involvement of genes previously implicated in preeclampsia development.

Earlier research suggested that preeclampsia happens when the mother's immune system starts to reject the placenta during pregnancy, treating it like an invading organism. This study provides a new link between the immune system and preeclampsia.

Preeclampsia causes high blood pressure and fluid retention during pregnancy, due to problems with the placenta, and can lead to problems with fetal development. It can also develop in rare cases to eclampsia, which is life threatening and associated with high maternal mortality.

Understanding more about the genetic mechanisms behind preeclampsia may lead to improved screening for the disorder. The study was published in the February 2011 issue of the journal Placenta.




SOURCES & REFERENCES
Genetic mechanism associated with preeclampsia
BJM | 17 February 2011

Comment from Professor James Walker, pre-eclampsia expert.

"Care needs to be taken before concluding any cause and effect (in this study), as changes seen may be as a result of the earlier changes in the invasion rather than the cause of it. ...This work adds to the increasing evidence of an immunological mediation in the disease, but still does not give us an answer or a potential treatment approach"