血红素加氧酶-1对星形胶质细胞和神经元对血红蛋白易感性的影响。
Effect of heme oxygenase-1 on the vulnerability of astrocytes and neurons to hemoglobin.
作者信息
Chen-Roetling Jing, Regan Raymond F
机构信息
Thomas Jefferson University, 1020 Sansom Street, Thompson 239, Philadelphia, PA 19107, USA.
出版信息
Biochem Biophys Res Commun. 2006 Nov 10;350(1):233-7. doi: 10.1016/j.bbrc.2006.09.036. Epub 2006 Sep 18.
Abstract
The heme oxygenase (HO) enzymes catalyze the rate-limiting step of heme breakdown. Prior studies have demonstrated that the vulnerability of neurons and astrocytes to hemoglobin is modified in cells lacking HO-2, the constitutive isoform. The present study assessed the effect of the inducible isoform, HO-1. Wild-type astrocytes treated for 3-5 days with 3-30 microM hemoglobin sustained no loss of viability, as quantified by LDH and MTT assays. The same treatment resulted in death of 25-50% of HO-1 knockout astrocytes, and a 4-fold increase in protein oxidation. Cell injury was attenuated by transfer of the HO-1 gene, but not by bilirubin, the antioxidant heme breakdown product. Conversely, neuronal protein oxidation and cell death after hemoglobin exposure were similar in wild-type and HO-1 knockout cultures. These results suggest that HO-1 induction protects astrocytes from the oxidative toxicity of Hb, but has no effect on neuronal injury.
摘要
血红素加氧酶（HO）催化血红素分解的限速步骤。先前的研究表明，在缺乏组成型异构体HO-2的细胞中，神经元和星形胶质细胞对血红蛋白的易损性会发生改变。本研究评估了诱导型异构体HO-1的作用。用3 - 30 microM血红蛋白处理3 - 5天的野生型星形胶质细胞，通过乳酸脱氢酶（LDH）和噻唑蓝（MTT）测定法量化，其活力没有损失。相同处理导致25% - 50%的HO-1基因敲除星形胶质细胞死亡，蛋白质氧化增加4倍。HO-1基因转移可减轻细胞损伤，但抗氧化血红素分解产物胆红素则不能。相反，在野生型和HO-1基因敲除培养物中，血红蛋白暴露后神经元蛋白质氧化和细胞死亡情况相似。这些结果表明，HO-1的诱导可保护星形胶质细胞免受血红蛋白的氧化毒性，但对神经元损伤没有影响。
相似文献
1
Effect of heme oxygenase-1 on the vulnerability of astrocytes and neurons to hemoglobin.血红素加氧酶-1对星形胶质细胞和神经元对血红蛋白易感性的影响。
Biochem Biophys Res Commun. 2006 Nov 10;350(1):233-7. doi: 10.1016/j.bbrc.2006.09.036. Epub 2006 Sep 18.
2
Cultured astrocytes from heme oxygenase-1 knockout mice are more vulnerable to heme-mediated oxidative injury.来自血红素加氧酶-1基因敲除小鼠的培养星形胶质细胞更容易受到血红素介导的氧化损伤。
J Neurosci Res. 2005 Dec 15;82(6):802-10. doi: 10.1002/jnr.20681.
3
Heme oxygenase-2 gene deletion increases astrocyte vulnerability to hemin.血红素加氧酶-2基因缺失增加了星形胶质细胞对血红素的易损性。
Biochem Biophys Res Commun. 2004 May 21;318(1):88-94. doi: 10.1016/j.bbrc.2004.03.187.
4
Heme oxygenase-2 gene deletion attenuates oxidative stress in neurons exposed to extracellular hemin.血红素加氧酶-2基因缺失减轻了暴露于细胞外血红素的神经元中的氧化应激。
BMC Neurosci. 2004 Sep 17;5:34. doi: 10.1186/1471-2202-5-34.
5
Adenoviral transfer of the heme oxygenase-1 gene protects striatal astrocytes from heme-mediated oxidative injury.腺病毒介导的血红素加氧酶-1基因转移可保护纹状体星形胶质细胞免受血红素介导的氧化损伤。
Neurobiol Dis. 2004 Nov;17(2):179-87. doi: 10.1016/j.nbd.2004.07.009.
6
Increasing expression of heme oxygenase-1 by proteasome inhibition protects astrocytes from heme-mediated oxidative injury.通过蛋白酶体抑制增加血红素加氧酶-1的表达可保护星形胶质细胞免受血红素介导的氧化损伤。
Curr Neurovasc Res. 2005 Jul;2(3):189-96. doi: 10.2174/1567202054368344.
7
Astrocyte-specific heme oxygenase-1 hyperexpression attenuates heme-mediated oxidative injury.星形胶质细胞特异性血红素加氧酶-1过度表达减轻血红素介导的氧化损伤。
Neurobiol Dis. 2007 Jun;26(3):688-95. doi: 10.1016/j.nbd.2007.03.006. Epub 2007 Mar 24.
8
Effect of targeted deletion of the heme oxygenase-2 gene on hemoglobin toxicity in the striatum.血红素加氧酶-2基因靶向缺失对纹状体血红蛋白毒性的影响。
J Cereb Blood Flow Metab. 2005 Nov;25(11):1466-75. doi: 10.1038/sj.jcbfm.9600143.
9
Heme oxygenase-2 knockout neurons are less vulnerable to hemoglobin toxicity.血红素加氧酶-2基因敲除的神经元对血红蛋白毒性的耐受性更强。
Free Radic Biol Med. 2003 Oct 15;35(8):872-81. doi: 10.1016/s0891-5849(03)00431-3.
10
Differential induction of heme oxygenase and other stress proteins in cultured hippocampal astrocytes and neurons by inorganic lead.无机铅对培养的海马星形胶质细胞和神经元中血红素加氧酶及其他应激蛋白的差异诱导作用。
Toxicol Appl Pharmacol. 2004 Jul 1;198(1):49-60. doi: 10.1016/j.taap.2004.03.001.
引用本文的文献
1
Korean Red Ginseng Improves Astrocytic Mitochondrial Function by Upregulating HO-1-Mediated AMPKα-PGC-1α-ERRα Circuit after Traumatic Brain Injury.韩国红参通过上调 HO-1 介导的 AMPKα-PGC-1α-ERRα 通路改善创伤性脑损伤后的星形胶质细胞线粒体功能。
Int J Mol Sci. 2021 Dec 3;22(23):13081. doi: 10.3390/ijms222313081.
2
Deferoxamine deconditioning increases neuronal vulnerability to hemoglobin.去铁胺预处理增加神经元对血红蛋白的易损性。
Exp Cell Res. 2020 May 1;390(1):111926. doi: 10.1016/j.yexcr.2020.111926. Epub 2020 Feb 26.
3
Hemopexin alleviates cognitive dysfunction after focal cerebral ischemia-reperfusion injury in rats.血红素结合蛋白减轻大鼠局灶性脑缺血再灌注损伤后的认知功能障碍。
BMC Anesthesiol. 2019 Jan 15;19(1):13. doi: 10.1186/s12871-019-0681-2.
4
A review on heme oxygenase-1 induction: is it a necessary evil.血红素加氧酶-1 诱导的研究进展：必要之恶？
Inflamm Res. 2018 Jul;67(7):579-588. doi: 10.1007/s00011-018-1151-x. Epub 2018 Apr 24.
5
Hemopexin increases the neurotoxicity of hemoglobin when haptoglobin is absent.当触珠蛋白缺失时，血红素结合蛋白会增加血红蛋白的神经毒性。
J Neurochem. 2018 Jun;145(6):464-473. doi: 10.1111/jnc.14328. Epub 2018 Apr 3.
6
Role of Carbon Monoxide in Neurovascular Repair Processing.一氧化碳在神经血管修复过程中的作用。
Biomol Ther (Seoul). 2018 Mar 1;26(2):93-100. doi: 10.4062/biomolther.2017.144.
7
CD163 Expression in Neurons After Experimental Intracerebral Hemorrhage.实验性脑出血后神经元中的CD163表达
Stroke. 2017 May;48(5):1369-1375. doi: 10.1161/STROKEAHA.117.016850. Epub 2017 Mar 30.
8
Targeting the Nrf2-Heme Oxygenase-1 Axis after Intracerebral Hemorrhage.脑出血后靶向Nrf2-血红素加氧酶-1轴
Curr Pharm Des. 2017;23(15):2226-2237. doi: 10.2174/1381612822666161027150616.
9
Haptoglobin increases the vulnerability of CD163-expressing neurons to hemoglobin.触珠蛋白增加了表达CD163的神经元对血红蛋白的易损性。
J Neurochem. 2016 Nov;139(4):586-595. doi: 10.1111/jnc.13720. Epub 2016 Jul 22.
10
Prion Protein-Hemin Interaction Upregulates Hemoglobin Synthesis: Implications for Cerebral Hemorrhage and Sporadic Creutzfeldt-Jakob Disease.朊病毒蛋白-血红素相互作用上调血红蛋白合成：对脑出血和散发性克雅氏病的影响
J Alzheimers Dis. 2016;51(1):107-21. doi: 10.3233/JAD-151039.
本文引用的文献
1
Systemic zinc protoporphyrin administration reduces intracerebral hemorrhage-induced brain injury.全身性给予锌原卟啉可减轻脑出血所致的脑损伤。
Acta Neurochir Suppl. 2006;96:232-6. doi: 10.1007/3-211-30714-1_50.
2
Inhibition of the ERK/MAP kinase pathway attenuates heme oxygenase-1 expression and heme-mediated neuronal injury.抑制细胞外信号调节激酶/丝裂原活化蛋白激酶（ERK/MAP）信号通路可减弱血红素加氧酶-1的表达及血红素介导的神经元损伤。
Neurosci Lett. 2006 May 8;398(3):230-4. doi: 10.1016/j.neulet.2006.01.003. Epub 2006 Jan 27.
3
Glutamate induces oxidative stress and apoptosis in cerebral vascular endothelial cells: contributions of HO-1 and HO-2 to cytoprotection.谷氨酸诱导脑血管内皮细胞氧化应激和凋亡：血红素加氧酶-1和血红素加氧酶-2对细胞保护的作用
Am J Physiol Cell Physiol. 2006 May;290(5):C1399-410. doi: 10.1152/ajpcell.00386.2005. Epub 2005 Dec 21.
4
Metalloporphyrins inactivate caspase-3 and -8.金属卟啉可使半胱天冬酶-3和-8失活。
FASEB J. 2005 Aug;19(10):1272-9. doi: 10.1096/fj.04-3259com.
5
Catalytically inactive heme oxygenase-2 mutant is cytoprotective.催化失活的血红素加氧酶-2突变体具有细胞保护作用。
Free Radic Biol Med. 2005 Aug 15;39(4):558-64. doi: 10.1016/j.freeradbiomed.2005.04.009.
6
Effect of targeted deletion of the heme oxygenase-2 gene on hemoglobin toxicity in the striatum.血红素加氧酶-2基因靶向缺失对纹状体血红蛋白毒性的影响。
J Cereb Blood Flow Metab. 2005 Nov;25(11):1466-75. doi: 10.1038/sj.jcbfm.9600143.
7
Astrocytes protect neurons from ethanol-induced oxidative stress and apoptotic death.星形胶质细胞可保护神经元免受乙醇诱导的氧化应激和凋亡性死亡。
J Neurosci Res. 2005 Jun 1;80(5):655-66. doi: 10.1002/jnr.20502.
8
Adenoviral transfer of the heme oxygenase-1 gene protects striatal astrocytes from heme-mediated oxidative injury.腺病毒介导的血红素加氧酶-1基因转移可保护纹状体星形胶质细胞免受血红素介导的氧化损伤。
Neurobiol Dis. 2004 Nov;17(2):179-87. doi: 10.1016/j.nbd.2004.07.009.
9
Heme oxygenase in experimental intracerebral hemorrhage: the benefit of tin-mesoporphyrin.实验性脑出血中的血红素加氧酶：锡-中卟啉的益处
J Neuropathol Exp Neurol. 2004 Jun;63(6):587-97. doi: 10.1093/jnen/63.6.587.
10
Heme oxygenase-2 gene deletion increases astrocyte vulnerability to hemin.血红素加氧酶-2基因缺失增加了星形胶质细胞对血红素的易损性。
Biochem Biophys Res Commun. 2004 May 21;318(1):88-94. doi: 10.1016/j.bbrc.2004.03.187.
Zotero 插件