Mid-late gestation leptin infusion induces placental mitochondrial and endoplasmic reticulum unfolded protein responses in a mouse model of preeclampsia.

ABSTRACT:

Introduction

Preeclamptic patients, both lean and obese, present with elevated leptin levels which are associated with the development of maternal endothelial dysfunction and adverse fetal outcomes, such as growth restriction, leading to low birth weight. Recent studies in pregnant mice demonstrate that mid-late gestation leptin infusion induces clinical characteristics of preeclampsia, including elevated maternal blood pressure, maternal endothelial dysfunction and fetal growth restriction. However, whether leptin triggers placental stress responses that contribute to adverse fetal outcomes as in preeclampsia is unknown.

Methods

In the current study we measured the expression of proteins involved in the endoplasmic reticulum (UPR^er) and mitochondrial (UPR^mt<

SUBMITTER: Faulkner JL 

PROVIDER: S-EPMC11631667 | biostudies-literature | 2024 Dec

REPOSITORIES: biostudies-literature