Hypoxia induces different genes in the lungs of rats compared with mice
Hypoxia induces different genes in the lungs of rats compared with mice
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DOI：
10.1152/physiolgenomics.00081.2001
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发表时间：
2003-02-06
影响因子：
4.6
通讯作者：
Geraci, MW
中科院分区：
文献类型：
--
作者：
Hoshikawa, Y;Nana-Sinkam, P;Geraci, MW
不同的动物物种对缺氧有不同的反应。小鼠在慢性缺氧暴露后肺动脉增厚的程度低于大鼠。我们推测，肺组织基因表达模式显示在缺氧大鼠将不同于缺氧小鼠。我们将Sprague-Dawley大鼠和C57 BL/6小鼠暴露于1周和3周的低压缺氧。尽管两个物种都发生了肺动脉高压，但小鼠的肺血管重塑比大鼠少。微阵列基因分析表明，当暴露于缺氧条件下，小鼠和大鼠之间的基因表达的不同模式。此外，一些基因似乎是更敏感的，在较早的时间点缺氧1周。大鼠的低血糖条件诱导参与内皮细胞增殖、细胞凋亡抑制和血管舒张的基因。暴露于低氧条件下的小鼠降低了参与血管舒张和内皮细胞增殖的基因的表达。虽然我们不能确定是否差异表达的基因在慢性缺氧的差异肺血管重塑的原因或后果，我们建议，一组选择性基因的过度和表达不足之间的平衡可能是负责肺血管重塑和血管张力控制。
Different animal species have a varying response to hypoxia. Mice develop less pulmonary artery thickening after chronic hypoxia exposure than rats. We hypothesized that the lung tissue gene expression pattern displayed in hypoxic rats would differ from that of hypoxic mice. We exposed Sprague-Dawley rats and C57BL/6 mice to both 1 and 3 wk of hypobaric hypoxia. Although both species developed pulmonary hypertension, mice showed less pulmonary vascular remodeling than rats. Microarray gene analysis demonstrated a distinct pattern of gene expression between mice and rats when exposed to hypoxic conditions. In addition, some genes appeared to be more responsive at an earlier time point of 1 wk of hypoxia. Hypoxic conditions in the rat induce genes involved in endothelial cell proliferation, repression of apoptosis, and vasodilation. Mice exposed to hypoxic conditions decrease the expression of genes involved in vasodilation and in endothelial cell proliferation. Although we cannot determine whether the differential expression of genes during chronic hypoxia is cause or consequence of the differential pulmonary vascular remodeling, we propose that a balance between over- and under-expression of a selective group of genes may be responsible for lung vascular remodeling and vascular tone control.