Effects of hypoxia and other injurious stimuli on collagen secretion and intracellular growth stimulating activity of bovine aortic smooth muscle cells in culture.

Effects of hypoxia and other injurious stimuli on collagen secretion and intracellular growth stimulating activity of bovine aortic smooth muscle cells in culture.
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缺氧和其他伤害性刺激对培养物中牛主动脉平滑肌细胞胶原蛋白分泌和细胞内生长刺激活性的影响。

DOI:
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发表时间:
1987
期刊:
Artery
影响因子:
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通讯作者:
A. Berg
A. Berg
中科院分区:
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文献类型:
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作者:
L. Stavenow;A. Berg

文献摘要

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将培养的牛动脉平滑肌细胞置于缺氧条件下孵育,测定缺氧期间和缺氧后细胞总DNA和胶原分泌量,以及缺氧细胞条件培养基对这些参数的影响。与对照组相比,缺氧时胶原蛋白分泌减少16.4%,缺氧后胶原蛋白分泌增加41.4%。两期后细胞总DNA显著降低。接受缺氧培养的条件培养基的新培养物显示,与对照组相比,胶原蛋白分泌增加了32.2%,而细胞总DNA没有改变。通过将SMC培养物暴露于缺氧或暴露于其他潜在的致动脉粥样硬化刺激的裂解细胞的上清液中,研究了先前显示从裂解培养的SMC中释放的生长刺激活性。通过将细胞置于缺氧环境中,或暴露于低密度脂蛋白或浓度高到足以导致细胞数量减少的香烟烟雾凝聚物中,可以增加每个细胞的生长刺激活性。提示上述作用可能有助于动脉粥样硬化发展过程中细胞增殖和胶原形成的增加。
Bovine arterial smooth muscle cells in culture were incubated in hypoxia and total cellular DNA and collagen secretion during and after the hypoxic period was measured as well as the effect of conditioned medium from hypoxic cells on these parameters. Collagen secretion decreased by 16.4% compared to controls during hypoxia but was increased by 41.4% in the post-hypoxic period. Total cellular DNA was significantly lower after both periods. New cultures, receiving conditioned medium from hypoxic cultures, showed an increased collagen secretion by 32.2% compared to controls while total cellular DNA was not changed. Growth stimulating activity, previously shown to be released from lysed cultured SMC, was assayed by exposing SMC cultures to supernatant from lysed cells that had been incubated in hypoxia or exposed to other potential atherogenic stimuli. The growth stimulating activity per cell could be increased by incubating cells in hypoxia, or exposing them to low density lipoproteins or cigarette smoke condensate in concentrations high enough to cause a decrease in cell number. It was suggested that the described effects might contribute to increased cell proliferation and collagen formation in the development of atherosclerosis.