SOD2 activity is not impacted by hyperoxia in murine neonatal pulmonary artery smooth muscle cells and mice.
SOD2 activity is not impacted by hyperoxia in murine neonatal pulmonary artery smooth muscle cells and mice.
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SOD2活性不会受到鼠新生儿肺动脉平滑肌细胞和小鼠的高氧影响。
DOI：
10.3390/ijms16036373
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发表时间：
2015-03-19
影响因子：
5.6
通讯作者：
Farrow KN
中科院分区：
文献类型：
--
作者：
Gupta A;Perez M;Lee KJ;Taylor JM;Farrow KN
25%的婴儿合并肺动脉高压（PH）和支气管肺发育不良（BPD）。超氧化物歧化酶2（SOD 2）是一种内源性线粒体抗氧化剂，过表达可保护成年小鼠免受急性肺损伤。C57 Bl/6小鼠和同基因SOD 2 +/+和SOD 2 −/+小鼠被置于室内空气（对照）或75% O2（慢性高氧，CH）中14天。以富尔顿指数评价右室肥厚（RVH）。在福尔马林固定的肺切片上评估中壁厚度（MWT）和肺泡面积。将肺动脉平滑肌细胞（PASMC）置于21%或95%O2中培养24 h。分析肺和PASMC蛋白的SOD 2表达和活性。氧化应激用神经靶向传感器mitoRoGFP测量。CH肺具有增加的SOD 2表达，但活性不变。SOD 2-/+ PASMC在基线时表达和活性降低，但在高氧下增加SOD 2表达。高氧可增加PASMC中SOD 2 +/+和SOD 2 −/+的线粒体ROS。SOD 2 +/+和SOD 2-/+ CH幼仔诱导SOD 2表达，但不诱导活性，并在RVH、MWT和肺泡面积方面产生等同的增加。由于SOD 2 −/+小鼠发生了相同的疾病，这表明其他抗氧化系统可能在高氧诱导的氧化应激期间补偿新生儿期的部分SOD 2表达和活性。
Pulmonary hypertension (PH) complicates bronchopulmonary dysplasia (BPD) in 25% of infants. Superoxide dismutase 2 (SOD2) is an endogenous mitochondrial antioxidant, and overexpression protects against acute lung injury in adult mice. Little is known about SOD2 in neonatal lung disease and PH. C57Bl/6 mice and isogenic SOD2+/+ and SOD2−/+ mice were placed in room air (control) or 75% O2 (chronic hyperoxia, CH) for 14 days. Right ventricular hypertrophy (RVH) was assessed by Fulton’s index. Medial wall thickness (MWT) and alveolar area were assessed on formalin fixed lung sections. Pulmonary artery smooth muscle cells (PASMC) were placed in 21% or 95% O2 for 24 h. Lung and PASMC protein were analyzed for SOD2 expression and activity. Oxidative stress was measured with a mitochondrially-targeted sensor, mitoRoGFP. CH lungs have increased SOD2 expression, but unchanged activity. SOD2−/+ PASMC have decreased expression and activity at baseline, but increased SOD2 expression in hyperoxia. Hyperoxia increased mitochondrial ROS in SOD2+/+ and SOD2−/+ PASMC. SOD2+/+ and SOD2−/+ CH pups induced SOD2 expression, but not activity, and developed equivalent increases in RVH, MWT, and alveolar area. Since SOD2−/+ mice develop equivalent disease, this suggests other antioxidant systems may compensate for partial SOD2 expression and activity in the neonatal period during hyperoxia-induced oxidative stress.
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影响因子：
2.9
作者：
Murthy, K.;Savani, R. C.;Evans, J. R.
通讯作者：
Evans, J. R.
胎儿生长限制和支气管肺发育不良的早产儿的肺部高血压。
影响因子：
2.9
作者：
Check, J.;Gotteiner, N.;Liu, X.;Su, E.;Porta, N.;Steinhorn, R.;Mestan, K. K.
通讯作者：
Mestan, K. K.
DOI：
10.1164/rccm.200902-0242oc
发表时间：
2009-12-01
影响因子：
24.7
作者：
Aslam, Muhammad;Baveja, Rajiv;Kourembanas, Stella
通讯作者：
Kourembanas, Stella
影响因子：
7.4
作者：
Gong, Y.;Yi, M.;Dakshinamurti, S.
通讯作者：
Dakshinamurti, S.
影响因子：
5.3
作者：
Guo, ZM;Yang, H;Richardson, A
通讯作者：
Richardson, A