Hypoxic up-regulation of triosephosphate isomerase expression in mouse brain capillary endothelial cells

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• 作者：Yamaji ; Ryoichi ; Fujita ; Kayoko ; Nakanishi ; Isao ; Nagao ; Kaori ; Naito ; Mikihiko ; Tsuruo ; Takashi ; et. al.
• 关键词：Hypoxia ; Triosephosphate isomerase ; Mouse brain capillary endothelial cells ; Intracellular Ca²⁺ ; Non-selective cation channels ; Na⁺/Ca²⁺ exchange ; AP-1
• 刊名：Archives of Biochemistry and Biophysics
• 出版年：2004
• 期刊代码：116_00039861
• 类别：ch
• 出版时间：March 15, 2004
• 卷：423
• 期：2
• 页码：332-342
• 文件大小：2.15 M

摘要

A protein with a molecular mass of 27kDa was induced by hypoxia in a mouse brain capillary endothelial cell line and identified as triosephosphate isomerase (TPI) by amino-terminal sequencing. Hypoxia caused an elevation of the TPI protein level, concomitant with an increase of the TPI mRNA level. However, hypoxia resulted in an insufficient elevation of TPI activity level, compared to an increase of TPI protein level. When cells expressing the recombinant TPI protein with histidine tag were exposed to hypoxia and the TPI protein was affinity-purified, the catalytic activity (specific activity) of the TPI protein purified from hypoxic cells was substantially lower than that obtained from normoxic cells. In addition, three TPI isoforms with an electrophoretic multiplicity were found; two of the three isoforms were substantially increased in response to the hypoxia, but the level of the most acidic isoform was barely changed. The induction of TPI gene expression by hypoxia was suppressed by (1) a chelator of intracellular Ca²⁺, (2) a blocker of non-selective cation channels, (3) a blocker of Na⁺/Ca²⁺ exchangers, (4) an inhibitor of Ca²⁺/calmodulin-dependent protein kinases, and (5) an inhibitor of c-jun/AP-1 activation.