Dissecting Cross-species Anatomical Divergence with In Vivo Perturb Seq Reveals Regulators of Collateral Artery Development
Event Details
- Type
- Friday Lecture Series
- Speaker(s)
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Kristy Red-Horse, Ph.D., professor of biology, department of biology, director of graduate studies for stem cell biology and regenerative medicine, Institute for Stem Cell Biology and Regenerative Medicine, Stanford University; investigator, Howard Hughes Medical Institute
- Speaker bio(s)
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Collateral arteries are natural bypasses that improve outcomes in coronary artery disease and stroke, yet the mechanisms driving their formation remain unclear. While arterial occlusions cause severe ischemia in humans and mice, guinea pigs possess abundant protective collateral networks, highlighting key species differences. To uncover genetic regulators, the Red-Horse Lab developed an in vivo Perturb-seq platform using CRISPR-interference in neonatal mouse brain endothelial cells, screening 162 cross-species candidate genes. The screen revealed known and novel pathways, converging on a hypoxia-responsive network. In vivo validation confirmed that targeting Wnt, metabolic, and chaperone pathways modulates collateral formation, revealing therapeutic targets for natural bypass growth.
Kristy Red-Horse, Ph.D., is a Professor in the Department of Biology and the Institute for Stem Cell Biology & Regenerative Medicine at Stanford University and an Investigator with the Howard Hughes Medical Institute. Her research focuses on the mechanisms of blood vessel development, regeneration, and repair. During her Ph.D., she investigated how the placental vasculature connects with the maternal circulation, and as a postdoctoral fellow, she identified the progenitors of coronary arteries. Her lab now studies coronary vessel formation and regeneration with the long-term goal of developing strategies to promote therapeutic vascular growth to treat heart disease.
- Open to
- Tri-Institutional