Tracking of Infused Mesenchymal Stem Cells in Injured Pulmonary Tissue in Atm -Deficient Mice

• Published in: Cells (Basel, Switzerland) Switzerland), 2020-06, Vol.9 (6), p.1444
• Main Authors: Baer, Patrick C, Sann, Julia, Duecker, Ruth Pia, Ullrich, Evelyn, Geiger, Helmut, Bader, Peter, Zielen, Stefan, Schubert, Ralf
• Format: Article
• Language: English
• Subjects: Animals; Ataxia; Ataxia telangiectasia; Ataxia Telangiectasia - complications; Ataxia Telangiectasia - pathology; bio imaging; Bioluminescence; Bone marrow; Bronchiectasis; Cell therapy; Communication; Disease Models, Animal; Experiments; Fibrosis; Genomic instability; Humans; Inflammation; Lung diseases; Lung Diseases - etiology; Lung Diseases - physiopathology; Lung Injury - etiology; Lung Injury - physiopathology; Mesenchymal stem cells; Mesenchymal Stem Cells - metabolism; mesenchymal stromal/stem cells; Mice; Mice, Transgenic; Morbidity; Parenchyma; Phenotypes; Polymerase chain reaction; qRT-PCR; Respiratory tract diseases; Software; Stem cell transplantation; Stem cells; tracking; Transgenic mice; Ventilators
• ISSN: 2073-4409; 2073-4409
• DOI: 10.3390/cells9061444

Pulmonary failure is the main cause of morbidity and mortality in the human chromosomal instability syndrome Ataxia-telangiectasia (A-T). Major phenotypes include recurrent respiratory tract infections and bronchiectasis, aspiration, respiratory muscle abnormalities, interstitial lung disease, and pulmonary fibrosis. At present, no effective pulmonary therapy for A-T exists. Cell therapy using adipose-derived mesenchymal stromal/stem cells (ASCs) might be a promising approach for tissue regeneration. The aim of the present project was to investigate whether ASCs migrate into the injured lung parenchyma of -deficient mice as an indication of incipient tissue damage during A-T. Therefore, ASCs isolated from luciferase transgenic mice (mASCs) were intravenously transplanted into -deficient and wild-type mice. Retention kinetics of the cells were monitored using in vivo bioluminescence imaging (BLI) and completed by subsequent verification using quantitative real-time polymerase chain reaction (qRT-PCR). The in vivo imaging and the qPCR results demonstrated migration accompanied by a significantly longer retention time of transplanted mASCs in the lung parenchyma of -deficient mice compared to wild type mice. In conclusion, our study suggests incipient damage in the lung parenchyma of -deficient mice. In addition, our data further demonstrate that a combination of luciferase-based PCR together with BLI is a pivotal tool for tracking mASCs after transplantation in models of inflammatory lung diseases such as A-T.