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Mechanisms of maternal obesity and feto-placental development in preeclampsia

Award Number: R01HD114145
ORGANIZATION: NATIONAL INSTITUTE OF CHILD HEALTH AND HUMAN DEVELOPMENT
OPDIV: NIH
AWARD CLASS: DISCRETIONARY
AWARD ACTIVITY TYPE: SCIENTIFIC/HEALTH RESEARCH (INCLUDES SURVEYS)
PERIOD OF PERFORMANCE START DATE: 08/01/2024
PERIOD OF PERFORMANCE END DATE: 05/31/2029

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Mechanisms of maternal obesity and feto-placental development in preeclampsia - Project Summary: Maternal obesity with increased circulating inflammatory markers can lead to adverse pregnancy outcomes, such as preeclampsia (PE). The clinical signs of PE include maternal hypertension and proteinuria during the second half of gestation. While PE presents later in pregnancy, its origins are thought to begin early in pregnancy or even before conception. Importantly, maternal hypertension only resolves after delivery of the placenta; therefore, it is widely accepted that abnormal placentation plays a causal role in PE pathogenesis, though the etiology of this is unknown. It is our hypothesis that maternal adiposity contributes to heightened inflammation and subsequent abnormal placental vascular development. The overarching goal of these proposed studies is to test the hypothesis that pro-inflammatory mediators produced by maternal adipose tissue (leptin) reduce pro- angiogenic immune cells and factors at the maternal-fetal interface. We will test our hypothesis in the BPH/5 mouse model of PE combining novel in vivo and ex vivo experiments. In Aim 1, we will determine if hyperleptinemia promotes decidual inflammation at the maternal-fetal interface in early pregnancy. Leptin- STAT3 inflammatory mediators will be measured in control+leptin mice and BPH/5 mice that have hyperleptinemia, which is attenuated with weight loss. In Aim 2, we will use single cell sequencing to isolate the source of decidual inflammation in these pregnancies as well as placental angiogenic deficiency. In Aim 3, offspring outcomes will be assessed to determine whether reversal of maternal obesity via pair-feeding prevents aberrant fetal cardiac angiogenesis and adult onset cardiometabolic dysfunction. These experiments will combine the gold standard radiotelemetric blood pressure recording with metabolic cages to ascertain cardiometabolic fitness in offspring when maternal hyperleptinemia is blunted and PE is prevented. These findings will provide groundbreaking prenatal mechanisms to prevent adult-onset cardiometabolic disease, hypertension, in PE born offspring.


Issue Date FY	Funding FY	Legal Entity Name	Legal Entity Address	Legal Entity City	Legal Entity State	Legal Entity Zip Code	Legal Entity COUNTY	Legal Entity COUNTRY	Assistance Listing	Award Code	Budget Year	Action Date	Action Type	Action Amount

Issue Date FY: 2025 ( Subtotal = $501,307 )
2025	2025	COLORADO STATE UNIVERSITY	601 S HOWES ST	FORT COLLINS	CO	80521	LARIMER	USA	Child Health and Human Development Extramural Research	000	2	5/9/2025	NON-COMPETING CONTINUATION	$501,307
														Subtotal = $501,307

Issue Date FY: 2024 ( Subtotal = $456,251 )
2024	2024	COLORADO STATE UNIVERSITY	601 S HOWES ST	FORT COLLINS	CO	80521	LARIMER	USA	Child Health and Human Development Extramural Research	000	1	7/29/2024	NEW	$456,251
														Subtotal = $456,251

Grand Total All Awards = $957,558

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Mechanisms of maternal obesity and feto-placental development in preeclampsia

Award Number: R01HD114145

ORGANIZATION: NATIONAL INSTITUTE OF CHILD HEALTH AND HUMAN DEVELOPMENT

OPDIV: NIH

AWARD CLASS: DISCRETIONARY

AWARD ACTIVITY TYPE: SCIENTIFIC/HEALTH RESEARCH (INCLUDES SURVEYS)

PERIOD OF PERFORMANCE START DATE: 08/01/2024

PERIOD OF PERFORMANCE END DATE: 05/31/2029

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