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Construction of a Human Aorta Smooth Muscle Cell Organ-On-A-Chip Model for Recapitulating Biomechanical Strain in the Aortic Wall
Published on: July 6, 2022
Mechanical stress and human aortic smooth muscle cell proliferation
H Kawaguchi1, T Ozaki, T Murakami
1Laboratory Medicine, Hokkaido University School of Medicine, Sapporo, Japan.
Experimental and Clinical Cardiology
|April 30, 2010
Summary
Human aortic smooth muscle cells possess a pressure-sensitive mechanosensor that triggers DNA synthesis. This cellular switch activates above 140 mmHg, involving pertussis toxin-sensitive pathways.
Area of Science:
- Cardiovascular Biology
- Cellular Mechanotransduction
- Molecular Cell Biology
Background:
- Mechanical forces, including pressure and flow, are critical regulators of cell hypertrophy and proliferation.
- Understanding cellular responses to mechanical stimuli is key to comprehending physiological and pathological processes.
Purpose of the Study:
- To investigate the existence of mechanosensors specifically responsive to pure atmospheric pressure, independent of shear or tensile stresses.
- To identify the pressure threshold and signaling pathways involved in pressure-induced cellular responses.
Main Methods:
- Utilized a pressure-loading apparatus to apply controlled atmospheric pressure to human aortic smooth muscle cells.
- Assessed DNA synthesis in response to varying pressure levels (120-200 mmHg).
- Investigated the role of pertussis toxin and specific kinase pathways (ERK, JNK, p38) in mediating the pressure response.
Main Results:
- Atmospheric pressure between 140-180 mmHg significantly increased DNA synthesis in a pressure-dependent manner.
- Pressures of 120 mmHg or lower did not induce significant changes in DNA synthesis.
- Pertussis toxin completely inhibited pressure-induced DNA synthesis at 200 mmHg.
- Extracellular signal-related kinase (ERK) and c-Jun N-terminal kinase (JNK) activities were stimulated by pressures exceeding 160 mmHg.
Conclusions:
- Human aortic smooth muscle cells possess a mechanosensing switch activated by pure atmospheric pressure above 140 mmHg, leading to DNA synthesis.
- The activation mechanism involves both pertussis toxin-sensitive and -insensitive pathways, with the former being responsive to high pure pressure.
- These findings elucidate a novel pressure-sensing mechanism in vascular smooth muscle cells with implications for cardiovascular health.
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