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Updated: Jun 28, 2026

Isolation of Primary Patient-specific Aortic Smooth Muscle Cells and Semiquantitative Real-time Contraction Measurements In Vitro
Published on: February 15, 2022
Norepinephrine reversibly regulates the proliferation and phenotypic transformation of vascular smooth muscle cells
Lei Jiao1, Min-Chen Wang, Ya-An Yang
1Department of First Clinical Hospital, Medical College, Suzhou University, Suzhou 215123, China.
Objective:
To investigate the effect of norepinephrine (NE) on the proliferation and phenotypic transformation of vascular smooth muscle cells (VSMCs) and the mechanisms underlying this effect.
Methods:
VSMCs were isolated from the rat abdominal aorta. VSMCs cultured in both serum-containing or in a serum-free medium were treated with NE, oxidized low-density lipoprotein (ox-LDL), alpha-adrenergic receptor agonist (alpha1-R(-)), beta1-adrenergic receptor antagonist (beta1-R(-)) and various combinations of these factors. VSMC proliferation was determined by bromodeoxyuridine (BrdU) assays. The mRNA expression level of HRG-1 and SM22 alpha were determined by reverse transcription-polymerase chain reaction (RT-PCR).
Results:
The expressions of HRG-1 and SM22 alpha mRNA in NE- or OX-LDL-treated VSMCs was down-regulated, and the proliferation of BrdU-labeled cells increased; the expression of the above mentioned genes in the VSMCs treated with a combination of NE, alpha1-R, and beta1-R was significantly up-regulated. However, NE was observed to up-regulate the expression of HRG-1 and SM22 alpha mRNA in serum-starved VSMCs.
Conclusion:
NE could reversibly regulate the proliferation and phenotypic transformation of VSMCs. This regulation might be mediated via its receptors.
Insights
Norepinephrine (NE) reversibly affects vascular smooth muscle cell (VSMC) proliferation and transformation, potentially through its receptors. This finding offers insights into VSMC regulation.
Area of Science:
- Cardiovascular Biology
- Cellular Physiology
- Pharmacology
Background:
- Vascular smooth muscle cells (VSMCs) play a critical role in vascular tone and integrity.
- Dysregulation of VSMC proliferation and phenotypic transformation contributes to cardiovascular diseases.
Purpose of the Study:
- To investigate the effects of norepinephrine (NE) on VSMC proliferation and phenotypic transformation.
- To elucidate the underlying mechanisms, including the role of adrenergic receptors.
Main Methods:
- VSMCs were isolated from rat aorta and cultured.
- Cells were treated with NE, oxidized low-density lipoprotein (ox-LDL), and adrenergic receptor modulators.
- Proliferation was assessed using bromodeoxyuridine (BrdU) assays.
- mRNA expression of HRG-1 and SM22 alpha was quantified via RT-PCR.
Main Results:
- NE and ox-LDL down-regulated HRG-1 and SM22 alpha mRNA, increasing VSMC proliferation.
- Combined NE, alpha1-R agonist, and beta1-R antagonist treatments significantly up-regulated gene expression.
- NE increased HRG-1 and SM22 alpha mRNA expression in serum-starved VSMCs.
Conclusions:
- Norepinephrine exhibits reversible regulatory effects on VSMC proliferation and phenotypic transformation.
- These regulatory actions are likely mediated through NE's interaction with its specific receptors.
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