%0 Figure %A Farkas, Daniela %A Kraskauskas, Donatas %A I. Drake, Jennifer %A A. Alhussaini, Aysar %A Kraskauskiene, Vita %A J. Bogaard, Harm %A D. Cool, Carlyne %A F. Voelkel, Norbert %A Farkas, Laszlo %D 2014 %T Proliferation and apoptosis in the lungs of AMD3100-treated SU5416/chronic hypoxia (SuHx) animals. %U https://plos.figshare.com/articles/figure/_Proliferation_and_apoptosis_in_the_lungs_of_AMD3100_treated_SU5416_chronic_hypoxia_SuHx_animals_/943324 %R 10.1371/journal.pone.0089810.g007 %2 https://plos.figshare.com/ndownloader/files/1397025 %K Anatomy and physiology %K cardiovascular system %K Circulatory physiology %K Model organisms %K Animal models %K rat %K Molecular cell biology %K Cellular types %K Endothelial cells %K cardiovascular %K Pulmonary vascular diseases %K Vascular biology %K apoptosis %K lungs %K amd3100-treated %K hypoxia %X

(A) Representative Western blot for proliferating cell nuclear antigen (PCNA) and cleaved caspase-3 in the lung tissue protein lysate of naïve control animals (n = 3), SuHx + vehicle (n = 6) and SuHx + AMD3100 treated rats (n = 6). β-actin was used as loading control. (B-C) Densitometric analysis indicates increased PCNA (B) and cleaved caspase-3 (C) protein levels in the lungs of SuHx + vehicle animals vs. controls, and that AMD3100 treatment significantly reduced PCNA and cleaved caspase-3 protein levels in the lungs of SuHx animals. Densitometric values were normalized vs. β-actin and expressed as n-fold of naïve controls. n = 3 animals per group for controls and n = 6 animals per group for SuHx + vehicle and SuHx + AMD3100 groups. * P<0.05 and ** P<0.01.

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