Sanda Predescu
Rush University, IL·Medicine & Clinical Research
Pulmonary arterial hypertension (PAH) is a deadly disease in which the arteries of the lungs narrow and thicken, raising blood pressure and straining the heart. It affects women more often than men, and estrogen alone does not explain why.
- Fields
Medicine & Clinical Research
Physiology
Genetics
- Topics
pulmonary arterial hypertension
pulmonary hypertension
sex differences
- Grants
- 1 known grant, through May 2027
What they work on
- Validate that Xist, a long non-coding RNA that silences one X chromosome in females, is more highly expressed and active in female pulmonary arterial hypertension lung tissue and pulmonary artery endothelial cells.
- Test whether sex-specific increases in the Elk1 transcription factor and cyclin A1, a cell-cycle protein, drive faster cell cycle progression and growth of female pulmonary artery endothelial cells.
- Determine how Xist's interactions with downstream partners such as Klf2, a factor that keeps vessel cells quiet, contribute to the stronger growth response of female endothelial cells.
- Investigate how EHITSN, the intersectin-1s fragment produced by granzyme B, interacts with nuclear factors, and test whether targeting Xist reduces vascular remodeling in the EHITSN mouse model.
More about the research
Genetic studies have often left out the sex chromosomes, and no animal model has captured the sex differences of the human disease. This project asks whether a gene on the X chromosome helps explain the female bias.
Why it matters
Pulmonary arterial hypertension has no cure, is nearly always fatal and strikes women more often than men. Explaining how Xist drives faster growth of female lung vessel cells could guide sex-specific diagnosis and treatment. Testing whether blocking Xist reduces vessel damage could point to a new therapeutic target for patients.
Known grants
From NIH and NSF research grants. Labs often have other funding we can't see.
Closest labs
Yuanjun Shen
Binghamton University, NY·Medicine & Clinical Research·Early-career
Examine how Vps34, an enzyme that drives smooth muscle overgrowth, is activated in PAH lung arteries through Akt-dependent loss of phosphorylation at Ser164, including candidate phosphatases identified by computer analysis.
Roberto Machado
University of Maryland, Baltimore, MD·Medicine & Clinical Research
Define how NAMPT, the enzyme that makes the metabolic signaling molecule NAD, controls metabolic reprogramming in pulmonary artery endothelial cells during the pulmonary hypertension response.
Jason Hong
University of California-Los Angeles, CA·Medicine & Clinical Research·Early-career
Define how asporin blocks both TGF-β and EGFR signaling and what controls its protein levels in PAH pulmonary artery smooth muscle cells, using receptor-binding, drug-synergy, protein-stability and ubiquitination assays.
The school
Rush University: 7 labs on PI Pages, $139M a year on research, 26 research doctorates a year.
Reach out
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