Cellular mechanisms of placenta stress driven inflammation in maternal hyperinsulinemia

Active Project Grant Awarded Last action

Award ID
F31HD119977
Recipient
Awarding agency
Obligated
$75,782

Award facts

Completion date 0% complete
Originally
Place of performance
Minnesota, USA

Award details come from USAspending.gov.

Description

As the agency reported it.

Abstract
Maternal obesity and gestational diabetes mellitus induce placental inflammation and increase susceptibility of offspring to develop metabolic dysfunction in adulthood. Both conditions are associated with hyperglycemia, dyslipidemia, and hyperinsulinemia. Limited studies have been performed to study the independent impact of hyperinsulinemia on the placenta. The long-term goal of this research is to understand the mechanisms of how maternal hyperinsulinemia contributes to placental inflammation. Our data suggests that maternal hyperinsulinemia, by itself, is sufficient to increase the presence of CD68+ macrophages and trigger apoptotic induced stress. We propose that maternally derived monocytes/macrophages are recruited in response to placental trophoblast stress and that these stress signals can contribute to resident macrophage polarization. Our central hypothesis is that maternal hyperinsulinemia independently promotes trophoblast stress, resulting in increased macrophages infiltration and proinflammatory polarization in the placenta by altering the paracrine interactions between trophoblasts and macrophages. The main objective of this proposal is to determine the origin of infiltrating macrophages within the placenta and delineate the crosstalk between trophoblast and macrophages under hyperinsulinemic stress. Specific aim 1 will determine whether elevated macrophages are maternally derived. Specific aim 2 will investigate how stressed trophoblasts in a hyperinsulinemic environment influences macrophage polarization. This F31 proposal is innovative because there are currently no studies assessing the independent effect of insulin on placenta health and immune cell composition. Successful completion of the proposal will provide mechanistic insight into how maternal hyperinsulinemia drives trophoblast stress, placental inflammation, and immune cell infiltration at the maternal-fetal interface. The proposal incorporates new and timely-needed training in conceptual knowledge in placental inflammation, maternal hyperinsulinemia, trophoblast stress, including technical skills such as special imaging techniques (confocal, spatialomics) and flow cytometry to identify functions of immune cells in the placenta. Effective communication, mentorship, and leadership will be essential for becoming a successful academic. The university of minnesota and department of integrative biology & physiology offer extensive resources and mentors to support the trainee in completing her F31 proposal and achieving her goals. This award will provide tracy her with mentored training from excellent faculty while working on dissertation research, and facilitate her development into a strong applicant for a postdoctoral position.

Transactions

Action Obligated Date
Amendment $37,891
Amendment $37,891
Original award $0

Quick answers

Who received award F31HD119977?

F31HD119977 was awarded to Regents Of The University Of Minnesota by National Institute of Child Health and Human Development (National Institutes of Health) on December 1, 2026.

How much is award F31HD119977 worth?

$75,782 has been obligated on F31HD119977.

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