Post Reply FAQ Members Login

maternal polymorphism plays a role in PE phenotype

The Preeclampsia Foundation does not necessarily endorse any research or news found in this forum, we just want to share what is out there. Please use your own discretion to evaluate any information you find here.

maternal polymorphism plays a role in PE phenotype

Postby caryn » Mon Sep 14, 2009 11:04 am

by caryn (10131 Posts), Mon Sep 14, 2009 11:04 am

Maternal endothelin-1 is elevated and correlates with the severity of blood pressure elevation in preeclampsia. The endothelin-1 is likely released from the maternal endothelium. Presence of T allele at 5665 position in maternal EDN1 gene is associated with higher endothelin-1 levels. Placental endothelin-1 synthesis is reduced in preeclampsia. The combination of elevated maternal and reduced placental endothelin-1 may be an adaptive response to reduced uteroplacental flow in preeclampsia.

http://www.ncbi.nlm.nih.gov/pubmed/19730395

Read in conjunction with the [url="http://www.preeclampsia.org/forum/viewtopic.php?t=36499"]study about 17-p[/url] that I just posted, this illustrates pretty nicely what we're up against here. First: it's genetic. Second: it's adaptive, and blocking it might not be the best idea. When there's not enough bloodflow into the placenta, doing things that lower the maternal blood pressure has the potential to compromise the placental perfusion, and thus the baby. This is why we have [url="http://www.smfm.org"]maternal-fetal medicine specialists[/url] to balance the competing demands of mother and baby -- delivery and blood pressure control are always appropriate therapy for the mother, but not for the baby -- and why this is such a difficult disease to treat or cure.

Information provided on this site is provided for informational purposes only and is not meant to substitute for the advice provided by your own physician or other medical professional. You should not use the information contained herein for diagnosing or treating a health problem or disorder, or prescribing any medication. The Preeclampsia Foundation presents all data as is, without any warranty of any kind, express or implied, and is not liable for its accuracy, for mistakes or omissions of any kind, nor for any loss or damage caused by a user's reliance on information obtained on the site. Professional opinions on this condition vary greatly. The Preeclampsia Foundation endorses no one course of treatment or "cure".
User avatar
caryn
Forum Moderator
 
Posts: 10131
Joined: Fri Jun 25, 2004 06:36 am

Re : maternal polymorphism plays a role in PE phenotype

Postby jules2 » Thu Sep 24, 2009 12:08 am

by jules2 (514 Posts), Thu Sep 24, 2009 12:08 am

My daughter died in utero very unexpectedly (I had an us showing normal umbilical artery blood flow only about 20 hours before death), and I have often wondered if lowering my blood pressure was a factor in this. Not that I am blaming the docs, they could not let me wander around with a BP of 190/100 untreated, and they only lowered it to about 150/90.
jules2
Registered User
 
Posts: 514
Joined: Sun Jul 19, 2009 06:26 am

Re : maternal polymorphism plays a role in PE phenotype

Postby jgrumet » Fri Sep 25, 2009 01:44 am

by jgrumet (520 Posts), Fri Sep 25, 2009 01:44 am

I have no idea what the heck that says...I need to learn research language.
jgrumet
Registered User
 
Posts: 520
Joined: Sun Sep 21, 2008 08:33 pm

Re : maternal polymorphism plays a role in PE phenotype

Postby caryn » Fri Oct 02, 2009 07:04 pm

by caryn (10131 Posts), Fri Oct 02, 2009 07:04 pm

Jamie, I didn't do a terribly good job of translating it. Because I skipped the translating bit and went on to riff on how it connected to other stuff. :-)

It says that they found a protein that's probably produced by the mother's bloodstream to be elevated, and in a dose-response relationship to blood pressure (the higher the level of maternal endothelin-1, the higher the blood pressure.)

The women with generally higher levels also had a mutation in the gene that codes for that protein, the sort of mutation they call a "genetic polymorphism". (The funky clotting genes a lot of us have are also like this. We think of them as neutral mutations, because they show up in a substantial portion of the population and wouldn't do that if they usually killed people. Something like 30% of the Caucasian population carries the MTHFR mutation, and usually it doesn't seem to contribute to earlier death than the more common form of the gene.)

DNA is just four bases (A, C, T, and G), and one had been swapped just at point 5665 in the gene for endothelin-1 -- so we know exactly how this polymorphism looks.

So in the preeclamptics, maternal endothelin-1 was elevated and placental endothelin-1 was reduced. That's probably because it raises the mother's blood pressure and lowers the baby's. If the problem is poor blood flow into the placenta -- because the placenta's shallowly implanted -- then what the placenta does is turn up the pressure on the mother's side by increasing levels of production of this protein, and turn it down on the baby's side by decreasing it, so that blood is being pushed across the interface and then, once it gets to the baby's side, there's no obstacle at all to free flow. I think of it as a gradient, like the body is trying to make a waterfall by lifting the mother's side and lowering the baby's side.

And that is very likely an adaptive response to the condition of poor blood flow encountered by the placenta. When it detects a problem with poor blood flow (probably when it runs short of oxygen it throws multiple biochemical switches on in response), the placenta manipulates the maternal blood pressure and the fetal blood pressure to maximise blood flow to the baby given the shallow implantation.

As we say, evolution is smarter than you are. :-)
User avatar
caryn
Forum Moderator
 
Posts: 10131
Joined: Fri Jun 25, 2004 06:36 am


Return to Announcements and Preeclampsia in the News

Who is online

Users browsing this forum: No registered users and 1 guest

cron