[Cyclin D1 is involved in human pulmonary artery smooth muscle cells proliferation and migration induced by cigarette

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Updated: Jun 13, 2026

In Vitro Model for Studying Differentiation and Changes of Multi-Omics on Murine Airway Epithelial Cells Stimulated with Cigarette Smoke Extract
09:07

In Vitro Model for Studying Differentiation and Changes of Multi-Omics on Murine Airway Epithelial Cells Stimulated with Cigarette Smoke Extract

Published on: July 12, 2024

Min Xiang1, Yong-Jian Xu, Xian-Sheng Liu

  • 1Department of Respiratory Medicine, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China.

Sheng Li Xue Bao : [Acta Physiologica Sinica]
|April 20, 2010
PubMed

Insights

Cigarette smoke extract (CSE) promotes human pulmonary artery smooth muscle cell (HPASMC) proliferation and migration by increasing cyclin D1. Suppressing cyclin D1 with antisense cyclin D1 (pIRES2-EGFP-ascyclin D1) can reduce these CSE-induced effects.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Pulmonary Medicine

Context:

  • Cigarette smoke extract (CSE) is a major contributor to pulmonary vascular diseases.
  • Human pulmonary artery smooth muscle cells (HPASMCs) play a critical role in regulating vascular tone and structure.
  • Understanding the molecular mechanisms underlying CSE-induced HPASMC dysfunction is crucial for developing therapeutic strategies.

Purpose:

  • To investigate the role of cyclin D1 in CSE-induced proliferation and migration of HPASMCs.
  • To determine if inhibiting cyclin D1 expression can attenuate the effects of CSE on HPASMCs.

Summary:

  • A eukaryotic expression vector for antisense cyclin D1 (pIRES2-EGFP-ascyclin D1) was successfully constructed and transfected into HPASMCs.
  • CSE significantly increased cyclin D1 mRNA and protein levels in HPASMCs.
  • Inhibition of cyclin D1 expression using pIRES2-EGFP-ascyclin D1 attenuated CSE-induced HPASMC proliferation and migration.

Impact:

  • Cyclin D1 is implicated as a key mediator in CSE-induced HPASMC proliferation and migration.
  • Targeting cyclin D1 may offer a potential therapeutic approach for managing CSE-related pulmonary vascular pathologies.
  • This study provides insights into the molecular mechanisms of smoking-induced vascular remodeling.

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