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Updated: Jan 28, 2026
Invasive Hemodynamic Assessment for the Right Ventricular System and Hypoxia-Induced Pulmonary Arterial Hypertension in Mice
Published on: October 24, 2019
Long non-coding RNA CASC2 suppresses pulmonary artery smooth muscle cell proliferation and phenotypic switch in
Junsong Gong1, Zujun Chen2, Yu Chen3
1Department of Anesthesiology, State Key Laboratory of Cardiovascular Disease, Fuwai Hospital, National Center for Cardiovascular Diseases, Chinese Academy of Medical Sciences & Peking Union Medical College, No.167 Beilishi Rd., Xicheng District, Beijing, 100037, China.
Background:
In this study, we aimed to investigate whether and how lncRNA CASC2 was involved in hypoxia-induced pulmonary hypertension (PH)-related vascular remodeling.
Methods:
The expression of lncRNAs or mRNAs was detected by qRT-PCR, and western blot analysis or immunochemistry was employed for detecting the protein expression. Cell number assay and EdU (5-ethynyl-2'-deoxyuridine) staining were performed to assess cell proliferation. Besides, flow cytometry and wound healing assay were employed for assessments of cell apoptosis and cell migration, respectively. Rat model of hypoxic PH was established and the hemodynamic measurements were performed. Hematoxylin and eosin (HE) and Masson's trichrome staining were carried out for pulmonary artery morphometric analysis.
Results:
The expression of lncRNA CASC2 was decreased in hypoxia-induced rat pulmonary arterial tissues and pulmonary artery smooth muscle cells (PASMCs). Up-regulation of lncRNA CASC2 inhibited cell proliferation, migration yet enhanced apoptosis in vitro and in vivo in hypoxia-induced PH. Western blot analysis and immunochemistry showed that up-regulation of lncRNA CASC2 greatly decreased the expression of phenotype switch-related marker α-SMA in hypoxia-induced PH. Furthermore, it was indicated by the pulmonary artery morphometric analysis that lncRNA CASC2 suppressed vascular remodeling of hypoxia-induced rat pulmonary arterial tissues.
Conclusion:
LncRNA CASC2 inhibited cell proliferation, migration and phenotypic switch of PASMCs to inhibit the vascular remodeling in hypoxia-induced PH.
Insights
Long non-coding RNA CASC2 (lncRNA CASC2) suppresses pulmonary hypertension (PH) by inhibiting vascular remodeling. Upregulating lncRNA CASC2 reduces cell proliferation and migration while promoting apoptosis in PH.
Area of Science:
- Cardiovascular Research
- Molecular Biology
- Pulmonary Medicine
Background:
- Pulmonary hypertension (PH) involves complex vascular remodeling.
- The role of long non-coding RNAs (lncRNAs) in PH pathogenesis is an area of active investigation.
- Hypoxia is a key trigger for PH-related vascular remodeling.
Purpose of the Study:
- To investigate the involvement and mechanism of lncRNA CASC2 in hypoxia-induced pulmonary hypertension (PH).
- To determine the effect of lncRNA CASC2 on pulmonary artery smooth muscle cell (PASMC) proliferation, migration, and apoptosis.
- To assess the impact of lncRNA CASC2 on vascular remodeling in a rat model of hypoxic PH.
Main Methods:
- Quantitative real-time PCR (qRT-PCR) and western blotting for gene and protein expression analysis.
- Cell proliferation assays (EdU staining) and apoptosis assessment (flow cytometry).
- In vivo studies using a rat model of hypoxic PH with hemodynamic measurements and histological analysis (HE, Masson's trichrome staining).
Main Results:
- lncRNA CASC2 expression was decreased in hypoxia-induced rat pulmonary arteries and PASMCs.
- Upregulation of lncRNA CASC2 inhibited PASMC proliferation and migration, and promoted apoptosis in vitro and in vivo.
- lncRNA CASC2 suppressed the phenotypic switch of PASMCs, indicated by decreased α-SMA expression.
- lncRNA CASC2 attenuated vascular remodeling in hypoxia-induced PH.
Conclusions:
- lncRNA CASC2 plays a protective role in hypoxia-induced PH.
- lncRNA CASC2 inhibits PASMC proliferation, migration, and phenotypic switch, thereby mitigating vascular remodeling.
- Targeting lncRNA CASC2 may represent a therapeutic strategy for PH.
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