Return to search

Characterization of APOL1 renal risk variant effects on placental function and preeclampsia

Racial disparities in maternal mortality in the United States are urgently in need of greater attention and research. The prevalence of preeclampsia is higher among African American women than White women by 1.7-fold, and African American women are three times more likely to die from preeclampsia complications. Among African American patients, Apolipoprotein L1 protein (APOL1) gene variants are known to be linked to increased risk for non-diabetic chronic kidney disease (CKD). The Sub-Saharan African population is particularly affected by these risk variants, and they also have one of the highest rates of preeclampsia in the world. Variants in the APOL1 gene are common, with about 40-50% of African American individuals carrying one variant, suggesting that APOL1 may underlie other health conditions that disproportionately affect patients of recent African origin, including preeclampsia.

Previous epidemiologic studies support an association between APOL1 variants in the fetus and preeclampsia risk. There are also indications that in the kidney podocytes, these variants increase the endoplasmic reticulum (ER) specific stress protein GRP78, also known to regulate trophoblast syncytialization in the placenta. Although previous studies are suggestive, the mechanisms by which APOL1 variants alter placental function to increase preeclampsia risk are not understood. We utilized immunofluorescence (IF) studies to probe APOL1 expression in first trimester placenta (6-7 weeks gestation), as well as reverse-transcription polymerase chain reaction (RT-PCR) and Western blot studies to probe basal expression of messenger ribonucleic acid (mRNA) and protein of both APOL1 and GRP78 in BeWo cells. Our results have laid the foundation for studies of the role APOL1 plays in the genesis of preeclampsia. / 2026-03-06T00:00:00Z

Identiferoai:union.ndltd.org:bu.edu/oai:open.bu.edu:2144/48349
Date06 March 2024
CreatorsNam, Janice JaeEun
ContributorsKuohung, Wendy
Source SetsBoston University
Languageen_US
Detected LanguageEnglish
TypeThesis/Dissertation

Page generated in 0.0017 seconds