Mana M Parast
University of California-San Diego, CA·Medicine & Clinical Research
The placenta forms the link between mother and fetus and controls the fetus's supply of oxygen and nutrients, yet it remains one of the least understood human organs. When it develops or functions poorly, pregnancies can end in miscarriage, preeclampsia (dangerously high blood pressure in pregnancy), fetal growth restriction (FGR), preterm birth or stillbirth.
- Fields
Medicine & Clinical Research
Biology
Microbiology & Immunology
- Topics
placenta
trophoblast
Trisomy 21
- Grants
- 4 known grants, through Jun 2028
What they work on
- Test whether villitis of unknown etiology (VUE) linked to fetal growth restriction has a distinct cellular profile of chronic immune responses and trophoblast or endothelial damage, using mass cytometry on banked placental tissue.
- Profile placental immune cells collected prospectively from pregnancies with VUE, with or without growth restriction, by mass cytometry to find signatures that could become diagnostic biomarkers for late-onset fetal growth restriction.
- Determine whether CDX2-positive villous cytotrophoblasts are a distinct, possibly more primitive progenitor state, using trophoblast stem cells and organoids from placentas or pluripotent stem cells plus single-cell and single-nucleus RNA sequencing.
- Define the role of CDX2, a developmental transcription factor, in trophectoderm formation and trophoblast differentiation, and characterize why Trisomy 21 cytotrophoblasts keep CDX2 and fail to form syncytiotrophoblast.
- Characterize placental lesions of maternal and fetal vascular malperfusion at the molecular level using digital spatial profiling and mass spectrometry of decellularized extracellular matrix to build a cellular and matrix atlas.
- Test whether term cytotrophoblasts respond to specific cell- and matrix-derived signals to divide or become syncytiotrophoblast or extravillous trophoblast, and whether preeclampsia stems from altered matrix and paracrine signaling.
- Systematically characterize decidual cells, including decidual natural killer (dNK) cells, in term and preterm births to define how the maternal immune environment differs in spontaneous preterm birth.
- Model dNK-extravillous trophoblast interactions in the dish by deriving matched maternal and placental induced pluripotent stem cells (iPSCs) and differentiating them into dNK cells and extravillous trophoblast.
More about the research
These projects study trophoblast, the placenta's own epithelial cells, and how trophoblast interacts with the mother's immune system. They combine placentas examined by pathologists after delivery with stem cell-based models and tools that profile single cells, tissue regions and proteins.
Why it matters
Placental dysfunction underlies many adverse pregnancy outcomes, including miscarriage, preeclampsia, fetal growth restriction, preterm birth and stillbirth. These projects could give clinicians cellular signatures for diagnosing dangerous villitis and late-onset growth restriction. Those signatures could help identify families at risk of recurrence in future pregnancies. The work may also explain why Trisomy 21 pregnancies face high rates of miscarriage and growth restriction, reveal mechanisms behind unexplained spontaneous preterm birth, and point to ways to harness the placenta's regenerative capacity.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Trophoblast progenitor heterogeneity and function in normal and Trisomy 21-affected placentae
NIH · Sep 2023 – Jun 2028
Identification of a cellular immune signature unique to clinically-significant villitis of unknown etiology
NIH · Aug 2025 – Jul 2027
Cellular Atlas of the Human Placenta: Structure-Function Relationships and their Implications for Placental Dysfunction
NIH · Sep 2021 – Jul 2027
Closest labs
Mariko Horii
University of California-San Diego, CA·Medicine & Clinical Research
Identify which stem cell-based culture method best reproduces the abnormal trophoblast differentiation seen in preeclamptic placentas, comparing approaches for modeling syncytiotrophoblast and extravillous trophoblast development.
Emily Adhikari
University of Texas Southwestern Medical Center, TX·Medicine & Clinical Research·Early-career
Define types of placental tissue damage in pregnancies with syphilis and correlate them with Treponema pallidum burden and newborn outcomes, compared with gestational age–matched healthy controls.
Thorold Theunissen
Washington University in St Louis, MO·Genetics
Map the signaling cascade during early primed-to-naïve conversion of human pluripotent stem cells using quantitative phosphoproteomics, to find ways to activate naïve genes without causing instability.
The school
University of California-San Diego: 84 labs on PI Pages, $1.9B a year on research, 637 research doctorates a year.
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