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Pressure stress stimulates aortic smooth muscle cell proliferation through angiotensin II receptor mediated signal transduction pathways

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Mechanical forces related to pressure and flow are important for cell hypertrophy and proliferation. We hypothesized the presence of mechanosensors that were solely sensitive to pure atmospheric pressure in the absence of shear and tensile stresses. A pressure-loading apparatus was set up to examine the effects of atmospheric pressure on human aortic smooth muscle cells. Pressure application of 140 to 180 mmHg produced DNA synthesis in a pressure-dependent manner. In contrast, pressure of 120 mmHg or less produced no significant change. Pertussis toxin completely inhibited the pressure-induced increase of DNA synthesis, under high pressure of 200 mmHg. Both extracellular signal-related kinase and c-Jun N-terminal kinase activities, but not p38 activity, were stimulated by pressure of more than 160 mmHg. ACE inhibitor inhibited cell proliferation under the pressure. It also inhibited ERKs expression, but the addition of AII on ACE inhibitor under the pressure could not recover the cell proliferation. Furthermore, the inactive ACE inhibitor suppressed the cell proliferation. There is a possibility that these agents, not mediated by angiotensin II receptors, directly suppress cell proliferation system in our experiment. In summary, HASMC have a mechanosensing cellular switch for DNA synthesis which is sensitive to pure atmospheric pressure. The molecular switch is activated by pressure of more than 140 mmHg. The mechanism of the inhibitory effect of ACE inhibitor on cell proliferation stimulated by pure pressure is under way in our laboratory.


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