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<p>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.</p>

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

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年7月23日

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  • Wei Gao,
  • Guoshang Yang,
  • Chunxiao Chen,
  • Jiajun Zhang,
  • Jing Lu,
  • Mingkun Hu,
  • Shengjun Liang,
  • Changchun Xie,
  • Ning Jiang

摘要

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.