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Updated: Jul 7, 2026

Isolation of Primary Patient-specific Aortic Smooth Muscle Cells and Semiquantitative Real-time Contraction Measurements In Vitro
Published on: February 15, 2022
Hsc70 regulates cell surface ASIC2 expression and vascular smooth muscle cell migration
Samira C Grifoni1, Susan E McKey, Heather A Drummond
1Department of Physiology and Biophysics, University of Mississippi Medical Center, 2500 North State St., Jackson, MS 39216, USA.
Acid-sensing ion channel 2 (ASIC2) inhibits vascular smooth muscle cell migration. Heat shock protein 70 (Hsc70) normally suppresses ASIC2, but reducing Hsc70 increases ASIC2 and decreases cell migration.
Area of Science:
- Physiology
- Molecular Biology
- Cell Biology
Background:
- Members of the degenerin (DEG)/epithelial Na(+) channel (ENaC)/acid-sensing ion channel (ASIC) family are implicated in vascular smooth muscle cell (VSMC) migration.
- Previous findings indicated that suppressing ASIC2 enhances VSMC migration, suggesting an inhibitory role for ASIC2.
Purpose of the Study:
- To investigate the hypothesis that ASIC2 inhibits VSMC migration by increasing its cell surface expression.
- To explore the role of heat shock protein 70 (Hsc70) in regulating ASIC2 expression and VSMC migration.
Main Methods:
- Utilized the chemical chaperone glycerol to enhance ASIC2 expression and cell surface localization in VSMCs.
- Employed gene silencing techniques to investigate the roles of ASIC2 and Hsc70 in VSMC migration.
- Assessed the impact of glycerol and Hsc70 manipulation on platelet-derived growth factor (PDGF)-bb-mediated VSMC migration.
Main Results:
- Glycerol treatment increased cytoplasmic and cell surface ASIC2 expression, leading to inhibited PDGF-bb-mediated VSMC migration.
- ASIC2 silencing abrogated the inhibitory effect of glycerol on VSMC migration, confirming ASIC2's role.
- Hsc70 silencing increased ASIC2 cell surface expression and inhibited VSMC migration, an effect dependent on ASIC2.
- These data indicate Hsc70 normally inhibits ASIC2 expression, and its removal enhances ASIC2, reducing VSMC migration.
Conclusions:
- ASIC2 functions as an inhibitor of VSMC migration.
- Hsc70 negatively regulates ASIC2 expression in VSMCs.
- The ASIC2-Hsc70 interaction presents a potential therapeutic target for vascular remodeling and injury processes.
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