Michelle Kossack
University of Cincinnati, OH·Pharmacology·Early-career
Pollutants in the environment account for 20 to 30% of known birth defects of the heart and also contribute to adult heart disease. The same contaminants harm the ovaries and may help explain rising infertility worldwide.
- Fields
Pharmacology
Physiology
Biology
- Topics
dioxin
environmental contaminants
reproductive toxicology
- Grants
- 1 known grant, through Nov 2028
What they work on
- Determine how much the ovary contributes to heart damage caused by TCDD (a dioxin pollutant) in female zebrafish exposed as juveniles.
- Identify cellular and molecular targets of TCDD that are unique to or shared between the zebrafish heart and ovary, using single-cell sequencing.
- Test whether TCDD-induced infertility in zebrafish results from disruption of the blood-follicle barrier, the protective layer around developing egg cells.
More about the research
The heart and ovary depend on each other. The heart delivers oxygen to the ovary, and the ovary makes estrogen, a hormone that protects the heart. Yet studies usually examine each organ alone, missing how damage to one may worsen the other. This project asks whether a pollutant that hits both organs harms the female heart partly by damaging the ovary.
Why it matters
Environmental pollutants contribute to congenital and adult heart disease and may be helping to drive rising infertility. Finding the cells and molecules through which dioxin (TCDD) damages both the heart and ovary could clarify how environmental exposures injure the heart. It could also help identify environmental causes of human infertility and point toward more effective treatments.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Amanda Kallen
University of Vermont, VT·Genetics
Chart the ovarian aging process in genetically diverse Collaborative Cross mouse strains with low Anti-Müllerian hormone and reduced fertility by measuring ovarian reserve, hormones, follicle development and molecular aging markers.
Zelieann Craig
University of Arizona, AZ·Physiology
Identify the tissues and molecular events that raise free fatty acid levels inside ovarian follicles of mice exposed to human-relevant phthalate mixtures, testing the role of the LXR-SREBP1c pathway that controls fat production.
Haodi Wu
University of Pittsburgh, PA·Genetics
Define how removing NIPBL changes heart-cell function and gene activity, using human iPSC-derived heart muscle cells with a dTAG degradation switch, functional assays and single-cell RNA sequencing.
The school
University of Cincinnati: 18 labs on PI Pages, $740M a year on research, 275 research doctorates a year.
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