Optical cryoimaging of mitochondrial redox state in bronchopulmonary-dysplasia injury models in mice lungs.

Publications // Sheibani Lab // Feb 01 2015

PubMed ID: 25694965

Author(s): MasoudiMotlagh M, Sepehr R, Sheibani N, Sorenson CM, Ranji M. Optical cryoimaging of mitochondrial redox state in bronchopulmonary-dysplasia injury models in mice lungs. Quant Imaging Med Surg. 2015 Feb;5(1):159-62. doi: 10.3978/j.issn.2223-4292.2014.12.04. PMID 25694965

Journal: Quantitative Imaging In Medicine And Surgery, Volume 5, Issue 1, Feb 2015

BACKGROUND 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.

METHODS 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.

RESULTS We observed a 47% and 26% decrease in the NADH redox in Bcl-2 deficient lungs, Bcl-2 -/- and Bcl-2 VE-cad, respectively.

CONCLUSIONS Thus, Bcl-2 deficiency is associated with a significant increase in oxidative stress contributing to reduced angiogenesis and enhanced pathogenesis of BPD.