Enzyme may explain preeclampsia symptoms in pregnant women
By ANIWednesday, January 5, 2011
WASHINGTON - Researchers have discovered that a significant increase of an enzyme in the blood vessels of pregnant women with preeclampsia could explain some of the symptoms associated with the condition, including hypertension, swelling and protein in the urine.
The findings, by Virginia Commonwealth University School of Medicine experts, could lead to a treatment for preeclampsia, which is one of the most significant health problems in pregnancy.
Preeclampsia is diagnosed when the mother develops high blood pressure and starts losing protein in her urine after 20 weeks of pregnancy.
In their study, the researchers reported a significant increase in an enzyme called MMP-1 in blood vessels of women with preeclampsia and an imbalance in collagen-regulating genes that favoured the breakdown of collagen.
MMP-1 is an enzyme produced in tissues under conditions of inflammation that acts to break down collagen.
“The increase in MMP-1 that we found would compromise the integrity of the mother’s blood vessels, which could explain two of the clinical symptoms of preeclampsia - edema and proteinuria,” said lead author Scott Walsh, professor in the VCU Department of Obstetrics and Gynecology.
The team also found that MMP-1 causes blood vessel contraction by activation of a receptor known as PAR1, which according to Walsh, could explain the hypertension, or high blood pressure, of women with preeclampsia.
“This finding may be especially important for preeclampsia because we found increased amounts of PAR1 in blood vessels of preeclamptic women as compared to normal pregnant women. MMP-1 activation of PAR1 is a totally new mechanism to explain hypertension,” he said.
PAR1 is best known for its role in the coagulation of blood, but it is not known for a role in hypertension, said Walsh.
Further, the team showed that neutrophils, or white blood cells, and neutrophil products increase MMP-1 and PAR1.
According to Walsh, neutrophil infiltration may be the cause of the increase in MMP-1 and PAR1 in blood vessels that leads to vessel dysfunction and clinical symptoms of preeclampsia.
“Activation of the PAR1 receptor by MMP-1 causes changes in the endothelial cells of blood vessels that we speculated could result in contraction of blood vessels. This new information provides a rationale for the use of PAR1 inhibitors to treat preeclampsia,” said Walsh.
The study is published in the January issue of The American Journal of Pathology. (ANI)
