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Peer-reviewedCC BYScientific Reports

A pilot single-cell RNA sequencing study of endothelial activation signatures in large benign prostatic hyperplasia

  • Wei Gao1
  • Guoshang Yang1
  • Chunxiao Chen2
  • Jiajun Zhang1
  • Jing Lu1
  • Mingkun Hu1
  • Shengjun Liang1
  • Changchun Xie1
  • Ning Jiang2
  1. 1Department of Urology, Guangzhou Liwan Central Hospital
  2. 2Department of Urology, Zhujiang Hospital, Southern Medical University
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Abstract

Benign prostatic hyperplasia (BPH) is common in aging men, but the endothelial compartment in enlarged prostates remains poorly defined. In this hypothesis-generating pilot study, we generated a single-cell RNA-seq dataset from six surgically obtained BPH specimens (three Large BPH and three Small BPH) and analyzed 56,912 cells; public datasets GSE290213 and GSE242249 were used for external context. We observed a higher sample-level fraction of Activated endothelial cells and a lower fraction of Venous-like endothelial cells in Large BPH, but these descriptive summaries were not designed for formal group inference. RNA velocity, graph ordering, and focused Slingshot/tradeSeq analyses nominated a putative endothelial-state ordering; concordance between graph pseudotime and latent time was modest (Spearman rho = 0.252). Variance decomposition suggested that AP-1/NF-κB activity was largely linked to endothelial-state composition, whereas selected IFN/HLA-II-associated programs showed stronger group-linked genetic context. MAGMA and TWAS did not support Activated endothelial markers or Large-up endothelial genes as the main genetic signal; broader stromal-vascular and HLA-related patterns were more consistent with the genetic data. These findings nominate endothelial activation signatures and a two-axis exploratory model for future validation in larger clinically annotated cohorts with protein-level testing.

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Cite

BibTeXRIS
BibTeX
@article{gao2026pilot,
  title = {{A pilot single-cell RNA sequencing study of endothelial activation signatures in large benign prostatic hyperplasia}},
  author = {Wei Gao and Guoshang Yang and Chunxiao Chen and Jiajun Zhang and Jing Lu and Mingkun Hu and Shengjun Liang and Changchun Xie and Ning Jiang},
  journal = {Scientific Reports},
  year = {2026},
  month = jul,
  doi = {10.1038/s41598-026-63751-1},
  url = {https://doi.org/10.1038/s41598-026-63751-1},
  note = {CC BY},
}
RIS
TY  - JOUR
TI  - A pilot single-cell RNA sequencing study of endothelial activation signatures in large benign prostatic hyperplasia
AU  - Wei Gao
AU  - Guoshang Yang
AU  - Chunxiao Chen
AU  - Jiajun Zhang
AU  - Jing Lu
AU  - Mingkun Hu
AU  - Shengjun Liang
AU  - Changchun Xie
AU  - Ning Jiang
PY  - 2026
DA  - 2026/07/01
JO  - Scientific Reports
DO  - 10.1038/s41598-026-63751-1
UR  - https://doi.org/10.1038/s41598-026-63751-1
AB  - Benign prostatic hyperplasia (BPH) is common in aging men, but the endothelial compartment in enlarged prostates remains poorly defined. In this hypothesis-generating pilot study, we generated a single-cell RNA-seq dataset from six surgically obtained BPH specimens (three Large BPH and three Small BPH) and analyzed 56,912 cells; public datasets GSE290213 and GSE242249 were used for external context. We observed a higher sample-level fraction of Activated endothelial cells and a lower fraction of Venous-like endothelial cells in Large BPH, but these descriptive summaries were not designed for formal group inference. RNA velocity, graph ordering, and focused Slingshot/tradeSeq analyses nominated a putative endothelial-state ordering; concordance between graph pseudotime and latent time was modest (Spearman rho = 0.252). Variance decomposition suggested that AP-1/NF-κB activity was largely linked to endothelial-state composition, whereas selected IFN/HLA-II-associated programs showed stronger group-linked genetic context. MAGMA and TWAS did not support Activated endothelial markers or Large-up endothelial genes as the main genetic signal; broader stromal-vascular and HLA-related patterns were more consistent with the genetic data. These findings nominate endothelial activation signatures and a two-axis exploratory model for future validation in larger clinically annotated cohorts with protein-level testing.
SN  - 2045-2322
ER  -