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Peer-reviewedCC BY 4.0PLOS One

A comprehensive full-length transcriptome landscape of cigarette smoke-exposed HASMCs reveals extensive remodeling of mRNA isoforms and regulatory networks

  • Wei Gou1
  • Lei Yang2
  • Shan Chen
  • Yulin Miao
  • Weiwei Wang
  • Hai Li
  • Zhipeng Hu
  1. 1Department of Vascular Surgery, General Hospital of Ningxia Medical University, Yinchuan City, Ningxia, China
  2. 2Department of Colorectal Surgery, General Hospital of Ningxia Medical University, Yinchuan City, Ningxia, China
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Abstract

Cigarette smoke extract (CSE) exerts paradoxical concentration-dependent effects on vascular smooth muscle cells, though the underlying isoform-level mechanisms remain unexplored. We employed Oxford Nanopore long-read sequencing to analyze the full-length transcriptome of human aortic smooth muscle cells after CSE treatment. We confirmed that low-concentration CSE (0.2%) slightly promoted cell viability while higher concentrations (0.4%−0.8%) induced dose-dependent suppression. Sequencing of 0.6% CSE (midpoint cytotoxicity)-treated cells revealed 11,222 novel transcripts and extensive post-transcriptional reprogramming, including: 1,866 upregulated transcripts involving ferroptosis and cell division; 493 downregulated transcripts in oxidative phosphorylation and glutathione metabolism; 1,753 alternative polyadenylation events mediating 3’UTR remodeling; and 269 alternative splicing events affecting cell cycle regulators and transcription factors (CREM, FOSL1, HBP1). Our study suggests that high-concentration CSE cytotoxicity is executed through coordinated post-transcriptional dysregulation, providing the first isoform-level perspective on smoking-induced vascular pathology and revealing previously unrecognized regulatory mechanisms in cigarette smoke-mediated vascular injury.

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Cite

BibTeXRIS
BibTeX
@article{gou2026comprehensive,
  title = {{A comprehensive full-length transcriptome landscape of cigarette smoke-exposed HASMCs reveals extensive remodeling of mRNA isoforms and regulatory networks}},
  author = {Wei Gou and Lei Yang and Shan Chen and Yulin Miao and Weiwei Wang and Hai Li and Zhipeng Hu},
  journal = {PLOS One},
  year = {2026},
  month = sep,
  doi = {10.1371/journal.pone.0354604},
  url = {https://doi.org/10.1371/journal.pone.0354604},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - A comprehensive full-length transcriptome landscape of cigarette smoke-exposed HASMCs reveals extensive remodeling of mRNA isoforms and regulatory networks
AU  - Wei Gou
AU  - Lei Yang
AU  - Shan Chen
AU  - Yulin Miao
AU  - Weiwei Wang
AU  - Hai Li
AU  - Zhipeng Hu
PY  - 2026
DA  - 2026/09/21
JO  - PLOS One
DO  - 10.1371/journal.pone.0354604
UR  - https://doi.org/10.1371/journal.pone.0354604
AB  - Cigarette smoke extract (CSE) exerts paradoxical concentration-dependent effects on vascular smooth muscle cells, though the underlying isoform-level mechanisms remain unexplored. We employed Oxford Nanopore long-read sequencing to analyze the full-length transcriptome of human aortic smooth muscle cells after CSE treatment. We confirmed that low-concentration CSE (0.2%) slightly promoted cell viability while higher concentrations (0.4%−0.8%) induced dose-dependent suppression. Sequencing of 0.6% CSE (midpoint cytotoxicity)-treated cells revealed 11,222 novel transcripts and extensive post-transcriptional reprogramming, including: 1,866 upregulated transcripts involving ferroptosis and cell division; 493 downregulated transcripts in oxidative phosphorylation and glutathione metabolism; 1,753 alternative polyadenylation events mediating 3’UTR remodeling; and 269 alternative splicing events affecting cell cycle regulators and transcription factors (CREM, FOSL1, HBP1). Our study suggests that high-concentration CSE cytotoxicity is executed through coordinated post-transcriptional dysregulation, providing the first isoform-level perspective on smoking-induced vascular pathology and revealing previously unrecognized regulatory mechanisms in cigarette smoke-mediated vascular injury.
SN  - 1932-6203
ER  -