Skip to content
DraconiticResearch
Search Sources API
203,234 studies31 sourcesUpdated 20 min ago
Peer-reviewedCC BYCell

Persistent and transient senescent cells contribute to brain-barrier development

  • Lauren Ashley Watson1
  • Zoe Adelsheim1
  • Mackenzie J. Carter1
  • Grace T. Carter1
  • Karen L. Jimenez-Reyes1
  • Huijie Du1
  • Ziqing Zhu1
  • David B. Berry2
  • Mia C. Paredez1
  • Rania H. Palaniappan1
  • John M. Augustine1
  • Hiruy S. Meharena3
  1. 1Department of Neurobiology, University of California, San Diego, La Jolla, CA, USA
  2. 2Department of Orthopedic Surgery, University of California, San Diego, La Jolla, CA, USA
  3. 3Department of Neurobiology, University of California, San Diego, La Jolla, CA, USA; Department of Molecular Biology, University of California, San Diego, La Jolla, CA, USA. Electronic address: [email protected]
Open at sourceDOICite

Abstract

Establishment of the blood-brain barrier (BBB) and blood-cerebrospinal fluid (CSF) barrier requires precise coordination between diverse cell types to protect and nourish the brain. Here, we identify developmentally programmed p21 + senescent cells that exhibit divergent senescence-associated features across these two brain interfaces in mice. In the choroid plexus (ChP), epithelial cells adopt a lifelong, non-inflammatory senescent state associated with CSF production and blood-CSF barrier integrity. In contrast, vascular endothelial cells and brain-resident macrophages transiently exhibit pro-inflammatory senescence profiles during brain vascularization, with reciprocal signaling linked to angiogenic patterning and extracellular matrix assembly. The ablation of p21 + cells during mid-gestation disrupts brain vascular patterning and ChP integrity, which results in hemorrhage, impaired CSF production, and ventricular collapse. These findings indicate that embryonic senescent cells adopt divergent transient and long-lived states that support brain-barrier formation and homeostasis, thus reframing the prevailing view of persistent senescence beyond solely a pathological state.

Related

  1. Vessel-associated microglia contribute to blood-brain barrier disruption via a Notch-IL-1β axis in the diabetic brain
    Da-Hye Lee, Min-Joo Jung, Han-Seok Jeong +4
    Scientific ReportsPeer-reviewedCC BY-NC-ND 4.0Full textNeurologyCrossref
  2. Transient tubular membrane injury is converted into persistent fibrosis through a macrophage-fibroblast relay
    P. Wang, Y. Ruan, T. Rao +3
    bioRxivPreprintAll rights reservedFull textGeneral medicinebioRxiv
  3. Fructose Promotes Oxidative Stress, Sphingolipid Remodelling and Transient Intestinal Barrier Dysfunction in Differentiated Caco-2 Cells
    Gabriele Serreli, Maria Melis, Claudia Guerriero +7
    NutrientsPeer-reviewedCC BY 4.0Full textEndocrinology & metabolismCrossrefEurope PMC
  4. Transient peripheral compression induces persistent central pain: the acute constriction injury model
    Kaixuan Luo, Xiangjun Feng, Yang Liu +9
    Frontiers in Systems NeurosciencePeer-reviewedCC BYFull textPhysiologyDOAJ
  5. Persistent cerebrospinal fluid tumor cells during transient radiographic response in bilateral retinoblastoma with central nervous system involvement: a pediatric case report.
    Jianjun Zhu, Chenghao Zhanghuang, Fengming Ji +5
    Translational pediatricsPeer-reviewedCC BY-NC-NDFull textGeneral medicineEurope PMC

Cite

BibTeXRIS
BibTeX
@article{watson2026persistent,
  title = {{Persistent and transient senescent cells contribute to brain-barrier development}},
  author = {Lauren Ashley Watson and Zoe Adelsheim and Mackenzie J. Carter and Grace T. Carter and Karen L. Jimenez-Reyes and Huijie Du and Ziqing Zhu and David B. Berry and Mia C. Paredez and Rania H. Palaniappan and John M. Augustine and Hiruy S. Meharena},
  journal = {Cell},
  year = {2026},
  month = jun,
  doi = {10.1016/j.cell.2026.05.022},
  url = {https://doi.org/10.1016/j.cell.2026.05.022},
  note = {CC BY},
}
RIS
TY  - JOUR
TI  - Persistent and transient senescent cells contribute to brain-barrier development
AU  - Lauren Ashley Watson
AU  - Zoe Adelsheim
AU  - Mackenzie J. Carter
AU  - Grace T. Carter
AU  - Karen L. Jimenez-Reyes
AU  - Huijie Du
AU  - Ziqing Zhu
AU  - David B. Berry
AU  - Mia C. Paredez
AU  - Rania H. Palaniappan
AU  - John M. Augustine
AU  - Hiruy S. Meharena
PY  - 2026
DA  - 2026/06/10
JO  - Cell
DO  - 10.1016/j.cell.2026.05.022
UR  - https://doi.org/10.1016/j.cell.2026.05.022
AB  - Establishment of the blood-brain barrier (BBB) and blood-cerebrospinal fluid (CSF) barrier requires precise coordination between diverse cell types to protect and nourish the brain. Here, we identify developmentally programmed p21 + senescent cells that exhibit divergent senescence-associated features across these two brain interfaces in mice. In the choroid plexus (ChP), epithelial cells adopt a lifelong, non-inflammatory senescent state associated with CSF production and blood-CSF barrier integrity. In contrast, vascular endothelial cells and brain-resident macrophages transiently exhibit pro-inflammatory senescence profiles during brain vascularization, with reciprocal signaling linked to angiogenic patterning and extracellular matrix assembly. The ablation of p21 + cells during mid-gestation disrupts brain vascular patterning and ChP integrity, which results in hemorrhage, impaired CSF production, and ventricular collapse. These findings indicate that embryonic senescent cells adopt divergent transient and long-lived states that support brain-barrier formation and homeostasis, thus reframing the prevailing view of persistent senescence beyond solely a pathological state.
SN  - 0092-8674
SN  - 1097-4172
ER  -