MasoudiMotlagh Mohammad, Sepehr Reyhaneh, Sheibani Nader, Sorenson Christine M, Ranji Mahsa
1 Biophotonics laboratory, University of Wisconsin Milwaukee, Department of Electrical Engineering and Computer Science, 3200 N Cramer St., Milwaukee, WI 53211, USA ; Departments of 2 Ophthalmology and Visual Sciences, and 3 Pediatrics, University of Wisconsin School of Medicine and Public Health, 1111 Highland Avenue, Madison, WI 53705, USA.
Quant Imaging Med Surg. 2015 Feb;5(1):159-62. doi: 10.3978/j.issn.2223-4292.2014.12.04.
Bronchopulmonary dysplasia (BPD) is a major cause of morbidity and mortality in premature infants exposed to high levels of oxygen. This is mainly attributed to increased oxidative stress and angiogenesis defects impacting lung alveolarization.
Here we use optical imaging to investigate the role of Bcl-2 in modulation of oxidative stress and angiogenesis and pathogenesis of BPD. Cryoimaging of the mitochondrial redox state of mouse lungs was applied to determine the metabolic state of the lungs from Bcl-2 +/+ (control), Bcl-2-deleted in the endothelium (Bcl-2 VE-cad) and Bcl-2-deficient (Bcl-2 -/-; global null) using mitochondrial metabolic coenzymes NADH (Nicotinamide Adenine Dinucleotide), and FADH2 (Flavin Adenine Dinucleotide) as the primary electron carriers in oxidative phosphorylation.
We observed a 47% and 26% decrease in the NADH redox in Bcl-2 deficient lungs, Bcl-2 -/- and Bcl-2 VE-cad, respectively.
Thus, Bcl-2 deficiency is associated with a significant increase in oxidative stress contributing to reduced angiogenesis and enhanced pathogenesis of BPD.
支气管肺发育不良（BPD）是暴露于高氧环境的早产儿发病和死亡的主要原因。这主要归因于氧化应激增加和影响肺泡化的血管生成缺陷。
在此，我们使用光学成像来研究Bcl-2在调节氧化应激、血管生成及BPD发病机制中的作用。应用小鼠肺线粒体氧化还原状态的低温成像，使用线粒体代谢辅酶烟酰胺腺嘌呤二核苷酸（NADH）和黄素腺嘌呤二核苷酸（FADH2）作为氧化磷酸化中的主要电子载体，来确定来自Bcl-2 +/+（对照）、内皮细胞中Bcl-2缺失（Bcl-2 VE-cad）和Bcl-2缺陷（Bcl-2 -/-；全身敲除）小鼠肺的代谢状态。
我们观察到，在Bcl-2缺陷肺（Bcl-2 -/-和Bcl-2 VE-cad）中，NADH氧化还原分别降低了47%和26%。
因此，Bcl-2缺陷与氧化应激显著增加相关，这导致血管生成减少并加剧了BPD的发病机制。
