Expression of bcl-2 and bax in regenerating rat renal tubules following ischemic injury
Expression of bcl-2 and bax in regenerating rat renal tubules following ischemic injury
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DOI：
10.1152/ajprenal.1997.272.5.f640
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发表时间：
1997-05-01
影响因子：
4.2
通讯作者：
Hammerman, MR
中科院分区：
文献类型：
--
作者：
Basile, DP;Liapis, H;Hammerman, MR
为了明确bcl-2和bax在成人肾脏中作为再生调节因子的潜在作用，它们的表达被表征为缺血后损伤。相对于假手术对照组大鼠肾脏中的水平，损伤后24 h内肾脏bcl-2 mRNA水平增加2.1倍。bcl-2 mRNA水平持续升高3天，但在缺血后第5天恢复到基线水平。假手术大鼠肾脏原位杂交显示bcl-2 mRNA在整个肾单位中弥漫性表达。肾损伤后，再生近曲小管细胞中bcl-2 mRNA表达明显增强，基底膜增厚。免疫组化结果显示bcl-2蛋白的定位与此相似。肾脏中Bax mRNA水平从缺血后24小时开始升高，并在损伤后7天保持升高。Bax mRNA和bax蛋白共定位于缺血后再生近端小管，并在乳头状增生中显著表达。结论：急性缺血性损伤后，肾脏bcl-2和bax表达增强，其变化具有可预测性。我们的研究结果表明，这些调节细胞凋亡发挥关键作用的过程中，受损的近端小管缺血后的修复。
To define potential roles for bcl-2 and bax in adult kidney as regulators of regeneration, their expressions were characterized postischemic injury. A 2.1-fold increase in levels of renal bcl-2 mRNA occurred within 24 h of injury relative to levels in kidney of sham-operated control rats. The levels of bcl-2 mRNA remained elevated for 3 days but returned to baseline by day 5 postischemia. In situ hybridization of kidneys from sham-operated rats demonstrated faint expression of bcl-2 mRNA localized diffusely throughout the nephron. After renal injury, the expression of bcl-2 mRNA was markedly enhanced in regenerating proximal tubule cells relining the basement membrane. Immunohistochemistry showed a similar localization for bcl-2 protein. Levels of bax mRNA in kidney were elevated beginning at 24 h postischemia and remained elevated for 7 days postinjury. Bax mRNA and bax protein were colocalized to regenerating proximal tubules postischemia and were prominently expressed in papillary proliferations. We conclude that the expressions of bcl-2 and bax in kidney are enhanced in a predictable pattern following acute ischemic injury. Our findings suggest that these regulators of apoptosis play key roles in the process of repair of the damaged proximal tubule postischemia.