Genetic ablation of Bach1 gene enhances recovery from hyperoxic lung injury in newborn mice via transient upregulation of inflammatory genes
Genetic ablation of Bach1 gene enhances recovery from hyperoxic lung injury in newborn mice via transient upregulation of inflammatory genes
复制标题
Bach1 基因的基因消融通过炎症基因的瞬时上调增强新生小鼠高氧肺损伤的恢复
作者：
Masato Ito;N. Nagano;Yukio Arai;Ryo Ogawa;Shingo Kobayashi;Yukiko Motojima;H. Go;M. Tamura;K. Igarashi;P. Dennery;Fumihiko Namba
背景：BTB和CNC同源物1（Bach 1）是血红素加氧酶（HO）-1的转录抑制因子。Bach 1破坏对新生小鼠高氧肺损伤的影响尚未确定。方法：将Bach 1 −/−和WT新生小鼠分别暴露于21%和95%的氧气中4 d，然后在室内空气中恢复。采用RT-PCR检测肺组织Bach 1、HO-1、白细胞介素（IL）-6和单核细胞趋化蛋白（MCP）-1 mRNA水平。肺炎症细胞因子水平测定使用流式细胞仪珠arrays.Results：新生儿高氧10天后恢复，Bach 1 −/−小鼠表现出改善肺泡化与WT相比。HO-1、IL-6和MCP-1 mRNA水平以及IL-6和MCP-1蛋白水平在暴露于新生儿高氧的Bach 1 −/−肺中显著升高。虽然在新生儿高氧后的Bach 1 −/−和WT肺中观察到细胞凋亡增加，但这些组之间的细胞凋亡没有差异。结论：Bach 1 −/−新生小鼠从高氧诱导的肺损伤中恢复良好。这种作用可能是通过HO-1的抗氧化/抗炎活性或促炎细胞因子的瞬时过表达来实现的。
Background:BTB and CNC homology 1 (Bach1) is a transcriptional repressor of heme oxygenase (HO)-1. The effects of Bach1 disruption on hyperoxic lung injury in newborn mice have not been determined. We aimed to investigate the role of Bach1 in the newborns exposed to hyperoxia.Methods:Bach1−/− and WT newborn mice were exposed to 21% or 95% oxygen for 4 d and were then allowed to recover in room air. Lung histology was assessed and lung Bach1, HO-1, interleukin (IL)-6, and monocyte chemoattractant protein (MCP)-1 mRNA levels were evaluated using RT-PCR. Lung inflammatory cytokine levels were determined using cytometric bead arrays.Results:After 10 d recovery from neonatal hyperoxia, Bach1−/− mice showed improved lung alveolarization compared with WT. HO-1, IL-6, and MCP-1 mRNA levels and IL-6 and MCP-1 protein levels were significantly increased in the Bach1−/− lungs exposed to neonatal hyperoxia. Although an increase in apoptosis was observed in the Bach1−/− and WT lungs after neonatal hyperoxia, there were no differences in apoptosis between these groups.Conclusion:Bach1−/− newborn mice were well-recovered from hyperoxia-induced lung injury. This effect is likely achieved by the antioxidant/anti-inflammatory activity of HO-1 or by the transient overexpression of proinflammatory cytokines.
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影响因子：
9.6
作者：
Vandivier, R. William;Henson, Peter M.;Douglas, Ivor S.
通讯作者：
Douglas, Ivor S.
在新生小鼠中沉默高氧诱导的 C/EBPα 可通过增强肺泡上皮细胞的增殖来改善肺结构。
DOI：
10.1152/ajplung.00082.2011
发表时间：
2011
期刊：
American journal of physiology. Lung cellular and molecular physiology
影响因子：
--
作者：
Yang,Guang;Hinson,MauriceD;Bordner,JessicaE;Lin,QingS;Fernando,AmalP;La,Ping;Wright,ClydeJ;Dennery,PhyllisA
通讯作者：
Dennery,PhyllisA
DOI：
10.1073/pnas.94.20.10919
发表时间：
1997-09-30
影响因子：
11.1
作者：
Poss, KD;Tonegawa, S
通讯作者：
Tonegawa, S
影响因子：
3
作者：
Jobe, Alan H.;Kallapur, Suhas G.
通讯作者：
Kallapur, Suhas G.
DOI：
10.1073/pnas.94.20.10925
发表时间：
1997-09-30
影响因子：
11.1
作者：
Poss, KD;Tonegawa, S
通讯作者：
Tonegawa, S