Format

Send to

Choose Destination
Pregnancy Hypertens. 2016 Oct;6(4):313-319. doi: 10.1016/j.preghy.2016.06.004. Epub 2016 Jun 30.

Trophoblast mitochondrial function is impaired in preeclampsia and correlates negatively with the expression of soluble fms-like tyrosine kinase 1.

Author information

1
Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA, United States. Electronic address: zzsengel@bidmc.harvard.edu.
2
Emory University, Atlanta, GA, United States.
3
Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA, United States.
4
Beth Israel Deaconess Medical Center and Harvard Medical School, Boston, MA, United States; Division of Maternal Fetal Medicine/ Obstetrics and Gynecology, University of Chicago Medical Center, Chicago, IL, United States.

Abstract

Preeclampsia is a common medical complication of pregnancy that is associated with significant morbidity and mortality to the mother and the baby. Extensive human epidemiological and experimental studies suggest that excess placental soluble fms-like tyrosine kinase 1, a potent anti-angiogenic factor leads to the maternal hypertension, proteinuria and other systemic complications of preeclampsia. To evaluate the mechanisms of the aberrant placental sFlt1 expression, we studied the role of mitochondrial dysfunction as one possible etiological factor. Here, using human placental samples, we demonstrate that both the activity and expression of a mitochondrial electron transport chain enzyme cytochrome C oxidase (COX) is diminished in the syncytiotrophoblast layer of the chorionic villi from preeclamptic subjects. In addition, there was an inverse correlation between mitochondrial COX enzyme activity and placental sFlt1 expression. Functional in situ enzyme chemistry with electron microscopy also confirmed impaired mitochondrial function in preeclampsia. Ultrastructural and morphometric analysis of mitochondria using electron microscopy demonstrated, that mitochondria are smaller in both the syncytiotrophoblast and cytotrophoblast layers of preeclamptic tissue. The etiology of the mitochondrial dysfunction in preeclampsia as a cause or effect of the placental anti-angiogenic state remains to be elucidated in future studies.

KEYWORDS:

Angiogenesis; Hypertension; Mitochondria; Oxidative stress; Preeclampsia

PMID:
27939475
DOI:
10.1016/j.preghy.2016.06.004
[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Elsevier Science
Loading ...
Support Center