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Evaluating the mechanism of heat-induced labor-associated signaling at the feto-maternal interface.

Award Number: R21HD121843
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: 08/15/2026
PERIOD OF PERFORMANCE END DATE: 07/31/2028

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Evaluating the mechanism of heat-induced labor-associated signaling at the feto-maternal interface. - Abstract Heat exposure during pregnancy is associated with an increased risk of preterm birth (PTB), one of the leading causes of neonatal morbidity and mortality. Despite increasing epidemiological evidence demonstrating this association, a knowledge gap remains in understanding the mechanistic pathways underlying heat-induced PTB. Pregnancy causes many physiological changes, including increased blood volume, fetal heat output, and metabolic rate, which may enhance sensitivity to heat. It is evident that heat exposure triggers increased maternal core body temperature, which may induce heat stress at feto-maternal interface tissues (FMi - placenta-decidua and fetal membranes-decidua) when contacted by maternal high body temperature. Heat stress at the FMi will likely trigger gene expression regulation and intercellular cross-talk changes. However, knowledge about key regulatory molecules associated with these changes is lacking. Potential candidates, such as small RNA, particularly microRNA (miRNA), are key post-transcriptional gene expression regulators and are considered essential in pregnancy maintenance. Heat-induced changes in gene regulation may impact the cellular proteome and be accompanied by altered FMi cell cross-talk, where extracellular vesicles (EVs; 30- 200 nm) and their cargo content may reflect or propagate cellular stress responses. Thus, we hypothesize that heat exposure activates stress-responsive signaling pathways at the FMi via miRNA-mediated post- transcriptional mechanisms and EV-based signaling. To address this hypothesis, we will utilize a developed humanized microphysiologic, multi-organ FMi on a chip that recreates both FMi architecture as in utero (interconnected fetal membrane/placental-decidual interfaces - FMi-PLA-OOC) to profile heat-induced miRNA and proteomic alterations. Initially, we will adapt the FMi-PLA-OOC with a dynamic microfluidic system that mimics physiological temperature distribution via maternal blood flow. This will be achieved through the perfusion of heated cell culture media (39°C) into the maternal compartment of the FMi-PLA-OOC. Next, we will perform integrated miRNA sequencing and quantitative proteomics to identify heat-responsive regulatory networks across maternal and fetal compartments. We will further investigate heat-induced changes in EVs by characterizing maternal and fetal-derived EVs' miRNA and protein cargo following heat exposure. Prior to EV cargo characterization, we will use placental alkaline phosphatase (PLAP) as a marker to differentiate maternal (PLAP-) and fetal (PLAP+) EV populations and proceed to profile their molecular contents to identify potential biomarkers of heat-associated PTB. This work will provide both mechanistic insights and candidate biomarkers, informing future diagnostic and therapeutic strategies. Our specific aims are: Aim 1A: Adaptation of FMi-PLA-OOC with a temperature-controlled dynamic flow system. Aim 1B: Integrating miRNA and proteomic profiling to identify heat-induced regulatory changes. Aim 2: Characterizing miRNA and protein cargo from maternal and fetal-derived EVs following heat exposure.


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: 2026 ( Subtotal = $440,000 )
2026	2026	UNIVERSITY OF TEXAS MEDICAL BRANCH AT GALVESTON	301 UNIVERSITY BLVD	GALVESTON	TX	77555	GALVESTON	USA	Child Health and Human Development Extramural Research	000	1	8/18/2026	NEW	$440,000
														Subtotal = $440,000

Grand Total All Awards = $440,000

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Evaluating the mechanism of heat-induced labor-associated signaling at the feto-maternal interface.

Award Number: R21HD121843

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: 08/15/2026

PERIOD OF PERFORMANCE END DATE: 07/31/2028

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