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Joyce E. Bischoff, Ph.D.

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Overview

Mentoring
Available: 09/03/24, Expires: 04/30/28

Infantile hemangioma (IH) is an extraordinary example of vascular overgrowth wherein vessels form rapidly, then undergo a slow spontaneous involution that leaves behind a fibrofatty residuum. IH is common: it occurs in 5% of infants, equating to ~183,200 infants/year in the U.S. alone. 10-15% of IH will cause complications – e.g. destroy facial structures and impair vision, breathing and feeding depending on the location. Propranolol was discovered serendipitously to be effective therapy for IH, yet some do not respond, regrowth occurs in ~20% of cases, and surgery is needed in 37% of patients to correct IH residua. REcently, we showed the non-beta blocker R+ enantiomers of propranolol and atenolol prevent hemangioma endothelial differentiation by directly interfering with the activity of the transcription factor SOX18 in hemangioma stem cells (HemSC). Further, R+ propranolol and R+ atenolol, along with a SOX18 small molecule inhibitor (Sm4), blocked hemangioma vessel formation in a pre-clinical model that uses IH patient derived HemSC. Our findings elucidate a novel etiological component of IH and validate a molecular target. Using R+ propranolol as a molecular probe, we uncovered by transcriptional profiling that the most coordinately decreased biological process during R (+) propranolol-mediated blockage HemSC endothelial differentiation is the mevalonate pathway. Furthermore, statins, which inhibit the rate limiting step in the mevalonate pathway, inhibit HemSC vessel formation in vivo. From this new data, we propose an entirely novel SOX18-mevalonate pathway axis as a central regulatory process in IH-vascular overgrowth. Our goals are to decipher how the SOX18-mevalonate pathway contributes to IH, investigate the gene regulatory networks that govern the vasculogenic and adipogenic transitions, and determine whether the SOX18-mevalonate axis is an etiological component in other vascular anomalies (VA), which could lead to further drug repurposing.

A Murine Model of Hemangioma using Cell-based Strategies
Summer, 03/29/04 - 01/04/04
Myeloid cell recruitment is necessary for bio-engineered vessel formation with ECFCs and MPCs in ischemic muscle
Summer, 06/06/12 - 07/25/12
Analysis of mRNA Expression During Cardiac Valve Epithelial-Mesenchymal Transformation
Summer, 06/19/00 - 08/14/00
Role of NFATcl in Control of Heart Valve Endothelial-mesenchymal Transformation
Part Time/Continuation, 09/01/00 - 12/31/00

Research
The research activities and funding listed below are automatically derived from NIH ExPORTER and other sources, which might result in incorrect or missing items. Faculty can login to make corrections and additions.
  1. T32HD104582 (GREENE, ARIN K.) May 9, 2022 - Apr 30, 2027
    NIH
    Pediatric Surgeon-Scientist Training Program in Vascular Diseases
    Role: Co-Principal Investigator
  2. R01HL141917 (LEVINE, ROBERT A) Apr 1, 2018 - Mar 31, 2022
    NIH
    Improving Mitral Compensation In Ischemic Regurgitation
    Role: Co-Principal Investigator
  3. R01HL127030 (BISCHOFF, JOYCE E.) Apr 1, 2016 - Jun 30, 2025
    NIH
    Capillary malformation: From somatic GNAQ mutations to disrupted endothelial biology
    Role: Principal Investigator
  4. R21AR063347 (BISCHOFF, JOYCE E.) Apr 1, 2013 - Mar 31, 2015
    NIH
    Building Vascularized Skeletal Muscle for Tissue Engineering/Regeneration
    Role: Co-Principal Investigator
  5. R01HL109506 (LEVINE, ROBERT A) May 15, 2012 - Apr 30, 2017
    NIH
    Improving Mitral Compensation in Ischemic Regurgitation
    Role: Co-Principal Investigator

Bibliographic
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Funded by the NIH National Center for Advancing Translational Sciences through its Clinical and Translational Science Awards Program, grant number UL1TR002541.