About

Panteleimon Rompolas is an Associate Professor of Dermatology at the University of Pennsylvania's Perelman School of Medicine. He also serves as the Associate Director of the Institute for Regenerative Medicine, specifically within the Epithelial Stem Cells Program. His educational background includes a B.S. in Biology from the University of Athens, Greece, obtained in 2001, and both a Ph.D. in Biomedical Science and an M.B.A. in Management from the University of Connecticut, completed in 2009. His research focuses on epithelial stem cells, their niches, and regenerative processes, with significant contributions to understanding the heterogeneity and dynamics of keratinocyte differentiation, as well as the mechanisms governing stem cell niche organization and function in skin and hair follicles. His work involves advanced imaging techniques, including intravital imaging, to study cellular behavior in vivo, and he has contributed to studies on nerve-dependent roles in wound re-epithelialization, hair cycle regulation, and primary cilia function in ocular tissues. His research has implications for regenerative medicine and tissue engineering, emphasizing the importance of innervation and cellular microenvironments in tissue regeneration.

Research topics

• Computer Science
• Neuroscience
• Cell biology
• Anatomy
• Biology

Selected publications

• Amelioration of Vascular Hyperpermeability Mediated by Targeted LNP Delivery of VE-Cadherin mRNA In Vivo

  Blood Advances · 2026-03-13

  articleOpen access

  Blood vessel hyperpermeability underlies a wide spectrum of potentially fatal diseases ranging from acute pulmonary edema to brain injuries such as ischemic stroke. Yet, effective strategies for rapid rehabilitation of the vascular endothelium to restore vascular homeostasis remain lacking. Here we developed an mRNA therapeutic encoding the vascular membrane structural protein VE-Cadherin (VEc), delivered via an anti-CD31 targeted lipid nanoparticle (aCD31/tLNP-VEc) directly to CD31+ vascular endothelial cells, for the quick restoration of vascular integrity. We showed that administration of a single dose of aCD31/tLNP-VEc significantly ameliorates pathological onsets in multiple mouse models of vascular hyperpermeability. In a bleomycin-induced lung edema model, we found aCD31/tLNP-VEc treatment significantly reduced fluid extravasation and decreased macrophage infiltrations. In a transient middle cerebral artery occlusion (tMCAO)-induced ischemic stroke model, aCD31/tLNP-VEc delivered post-injury diminished plasma protein leakage from brain edema by 50%. Targeted LNP-mediated delivery of VEc mRNA to the vascular network presents a promising platform for treating clinically relevant conditions involving vascular disruption.

  PublisherOA PDFDOI

• Stress vesicles link epidermal mechanotransduction to stem cell differentiation

  Nature Communications · 2026-01-23

  articleOpen accessSenior authorCorresponding

  The skin exhibits extraordinary plasticity, enabling it to adapt to mechanical changes in the environment. While transient deformations are accommodated without lasting structural effects, sustained mechanical stress induces durable tissue changes. To investigate if these responses are mediated by shifts in epidermal stem cell fate, we employed two-photon intravital imaging to visualize epidermal cells in live skin subjected to acute mechanical forces. Mechanical force triggered the formation of intracellular “stress” vesicles within epidermal stem cells that filled with extracellular fluid and progressively enlarged, deforming the nucleus. Lineage tracing analyses revealed that the extent of nuclear deformation can predict cell fate outcomes. Moreover, mechanical stress caused sustained elevation of intracellular calcium in basal epidermal stem cells, and conditional deletion of the mechanosensitive ion channel Piezo1 disrupted calcium dynamics and increased stress vesicle formation. Using human skin xenografts, we demonstrated that stress vesicles are conserved in mammalian skin. Together, these findings identify stress vesicles as key mediators linking mechanical stress, calcium signaling, and epidermal stem cell fate. Using two-photon intravital imaging, the authors show that mechanical stress in skin triggers fluid-filled “stress vesicles” in epidermal cells, altering Piezo1-dependent calcium signals to drive stem cell differentiation and protect tissue integrity.

  PublisherDOI

• Cell confinement initiates a delayed but heritable loss of chromosomes

  Cell Reports · 2026-03-01

  articleOpen access

  Heritable genetic changes continually arise in cancer, especially in solid tumors where cells are sometimes compressed. Rare heritable losses of chromosomes in live cells are quantified here with chromosome reporters (ChReporters), which reveal losses only after imposing a threshold level of confinement. Compression to ∼60% of interphase height ruptures few nuclei compared to deeper compression but perturbs mitotic spindles and prolongs pro/metaphase. Chromosome mis-segregation into micronuclei is discovered only after release from modest confinement, but arrest and death predominate. All such effects are phenocopied by nocodazole washout, which generates a "memory" of prolonged mitosis. The effects also differ from the rapid induction of micronuclei by a spindle-assembly checkpoint inhibitor and by a clinical CDK4/6 inhibitor of cell-cycle entry. Single-cell RNA sequencing confirms chromosome loss days after confinement and reveals dysregulation of chromosome-segregation pathways. Chromosome losses as mitotic memories of confinement ultimately address knowledge gaps in mechanobiology and cancer evolution.

  PublisherOA PDFDOI

• Cell confinement initiates a delayed but heritable loss of chromosomes

  bioRxiv (Cold Spring Harbor Laboratory) · 2026-02-03

  articleOpen access

  SUMMARY Heritable genetic changes continually arise in cancer, especially in solid tumors where cells sometimes appear compressed. Rare heritable losses of chromosomes in live cells are quantified here with chromosome reporters (ChReporters) that reveal similar levels of loss after imposing a threshold level of confinement. Compression to ∼60% of interphase height ruptures few nuclei compared to deeper compression but perturbs mitotic spindles and prolongs pro/metaphase. Chromosome mis-segregation into micronuclei is discovered only after release from modest confinement, but arrest and death predominate. All such effects are phenocopied by Nocodazole washout that generates a ‘memory’ of prolonged mitosis, and effects differ from the rapid induction of micronuclei by a spindle assembly checkpoint inhibitor and by a clinical CDK4/6-inhibitor of cell cycle entry. Single-cell-RNA-sequencing confirms chromosome loss days after confinement and reveals persistence of chromosome segregation pathways. Chromosome losses as mitotic memories of confinement ultimately address knowledge gaps in mechanobiology and cancer evolution.

  PublisherDOI

• 0778 Biomarkers of UV irradiated notch-deficient keratinocytes driving neoplasia

  Journal of Investigative Dermatology · 2025-07-21

  article
  PublisherDOI

• Author Correction: Tissue-scale coordination of cellular behaviour promotes epidermal wound repair in live mice

  Nature Cell Biology · 2025-11-10

  erratumOpen access
  PublisherOA PDFDOI

• Sox9 marks limbal stem cells and is required for asymmetric cell fate switch in the corneal epithelium

  bioRxiv (Cold Spring Harbor Laboratory) · 2024-04-11 · 7 citations

  preprintOpen accessSenior authorCorresponding

  Adult tissues with high cellular turnover require a balance between stem cell renewal and differentiation, yet the mechanisms underlying this equilibrium are unclear. The cornea exhibits a polarized lateral flow of progenitors from the peripheral stem cell niche to the center; attributed to differences in cellular fate. To identify genes that are critical for regulating the asymmetric fates of limbal stem cells and their transient amplified progeny in the central cornea, we utilized an in vivo cell cycle reporter to isolate proliferating basal cells across the anterior ocular surface epithelium and performed single-cell transcriptional analysis. This strategy greatly increased the resolution and revealed distinct basal cell identities with unique expression profiles of structural genes and transcription factors. We focused on Sox9; a transcription factor implicated in stem cell regulation across various organs. Sox9 was found to be differentially expressed between limbal stem cells and their progeny in the central corneal. Lineage tracing analysis confirmed that Sox9 marks long-lived limbal stem cells and conditional deletion led to abnormal differentiation and squamous metaplasia in the central cornea. These data suggest a requirement for Sox9 for the switch to asymmetric fate and commitment toward differentiation, as transient cells exit the limbal niche. By inhibiting terminal differentiation of corneal progenitors and forcing them into perpetual symmetric divisions, we replicated the Sox9 loss-of-function phenotype. Our findings reveal an essential role for Sox9 for the spatial regulation of asymmetric fate in the corneal epithelium that is required to sustain tissue homeostasis.

  PublisherOA PDFDOI

• Sox9 marks limbal stem cells and is required for asymmetric cell fate switch in the corneal epithelium

  eLife · 2024-09-02 · 1 citations

  preprintOpen accessSenior author

  Abstract Adult tissues with high cellular turnover require a balance between stem cell renewal and differentiation, yet the mechanisms underlying this equilibrium are unclear. The cornea exhibits a polarized lateral flow of progenitors from the peripheral stem cell niche to the center; attributed to differences in cellular fate. To identify genes that are critical for regulating the asymmetric fates of limbal stem cells and their transient amplified progeny in the central cornea, we utilized an in vivo cell cycle reporter to isolate proliferating basal cells across the anterior ocular surface epithelium and performed single-cell transcriptional analysis. This strategy greatly increased the resolution and revealed distinct basal cell identities with unique expression profiles of structural genes and transcription factors. We focused on Sox9; a transcription factor implicated in stem cell regulation across various organs. Sox9 was found to be differentially expressed between limbal stem cells and their progeny in the central corneal. Lineage tracing analysis confirmed that Sox9 marks long-lived limbal stem cells and conditional deletion led to abnormal differentiation and squamous metaplasia in the central cornea. These data suggest a requirement for Sox9 for the switch to asymmetric fate and commitment toward differentiation, as transient cells exit the limbal niche. By inhibiting terminal differentiation of corneal progenitors and forcing them into perpetual symmetric divisions, we replicated the Sox9 loss-of-function phenotype. Our findings reveal an essential role for Sox9 for the spatial regulation of asymmetric fate in the corneal epithelium that is required to sustain tissue homeostasis.

  PublisherOA PDFDOI

• 847 Biomarkers of early UV-induced skin cancer

  Journal of Investigative Dermatology · 2024-07-19

  articleOpen access
  PublisherOA PDFDOI

• Sox9 marks limbal stem cells and is required for asymmetric cell fate switch in the corneal epithelium

  eLife · 2024-09-02 · 3 citations

  preprintOpen accessSenior author

  Abstract Adult tissues with high cellular turnover require a balance between stem cell renewal and differentiation, yet the mechanisms underlying this equilibrium are unclear. The cornea exhibits a polarized lateral flow of progenitors from the peripheral stem cell niche to the center; attributed to differences in cellular fate. To identify genes that are critical for regulating the asymmetric fates of limbal stem cells and their transient amplified progeny in the central cornea, we utilized an in vivo cell cycle reporter to isolate proliferating basal cells across the anterior ocular surface epithelium and performed single-cell transcriptional analysis. This strategy greatly increased the resolution and revealed distinct basal cell identities with unique expression profiles of structural genes and transcription factors. We focused on Sox9; a transcription factor implicated in stem cell regulation across various organs. Sox9 was found to be differentially expressed between limbal stem cells and their progeny in the central corneal. Lineage tracing analysis confirmed that Sox9 marks long-lived limbal stem cells and conditional deletion led to abnormal differentiation and squamous metaplasia in the central cornea. These data suggest a requirement for Sox9 for the switch to asymmetric fate and commitment toward differentiation, as transient cells exit the limbal niche. By inhibiting terminal differentiation of corneal progenitors and forcing them into perpetual symmetric divisions, we replicated the Sox9 loss-of-function phenotype. Our findings reveal an essential role for Sox9 for the spatial regulation of asymmetric fate in the corneal epithelium that is required to sustain tissue homeostasis.

  PublisherDOI

Recent grants

• Live imaging of stem cell dynamics in cornea regeneration

  NIH · $2.0M · 2019–2025

Frequent coauthors

• Paola Kuri

  California University of Pennsylvania

  30 shared

• Gabriella Rice

  California University of Pennsylvania

  26 shared

• Sixia Huang

  University of Pennsylvania

  23 shared

• Olivia Farrelly

  California University of Pennsylvania

  18 shared

• Valentina Greco

  Yale University

  16 shared

• Vivian Lee

  University of Pennsylvania

  15 shared

• Tzvete Dentchev

  University of Pennsylvania

  13 shared

• Christopher J. Lengner

  California University of Pennsylvania

  13 shared

Labs

• Rompolas LabPI

Education

• Ph.D., Biomedical

  University of Connecticut Health Center

  2009

• M.B.A.

  University of Connecticut School of Business

  2009

• B.Sc., Biology

  National and Kapodistrian University of Athens

  2001