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Zfp148 Deficiency Causes Lung Maturation Defects and Lethality in Newborn Mice That Are Rescued by Deletion of p53 or Antioxidant Treatment

Journal article
Authors Volkan I. Sayin
Anna Nilton
Mohamed X Ibrahim
Pia Ågren
Erik Larsson
Marleen MR Petit
Lillemor Mattsson Hultén
Marcus Ståhlman
Bengt R Johansson
Martin Bergö
Per Lindahl
Published in Plos One
Volume 8
Issue 2
Pages e55720
ISSN 1932-6203
Publication year 2013
Published at Wallenberg Laboratory
Sahlgrenska Cancer Center
Institute of Biomedicine, Department of Medical Biochemistry and Cell Biology
Institute of Medicine, Department of Molecular and Clinical Medicine
Pages e55720
Language en
Keywords Animals, Animals, Newborn, Antioxidants, pharmacology, Apoptosis, Blotting, Southern, Blotting, Western, Cell Cycle, Cell Proliferation, Cells, Cultured, DNA-Binding Proteins, physiology, Embryo, Mammalian, cytology, drug effects, metabolism, Female, Fibroblasts, cytology, drug effects, metabolism, Gene Deletion, Genes, Lethal, Immunoenzyme Techniques, Lung, drug effects, embryology, metabolism, Mice, Mice, Inbred C57BL, Mice, Knockout, Oxidative Stress, drug effects, RNA, Messenger, genetics, Real-Time Polymerase Chain Reaction, Respiratory Tract Diseases, genetics, pathology, prevention & control, Reverse Transcriptase Polymerase Chain Reaction, Transcription Factors, physiology, Tumor Suppressor Protein p53, deficiency, genetics
Subject categories Cell and Molecular Biology, Clinical Medicine


The transcription factor Zfp148 (Zbp-89, BFCOL, BERF1, htβ) interacts physically with the tumor suppressor p53 and is implicated in cell cycle control, but the physiological role of Zfp148 remains unknown. Here we show that Zfp148 deficiency leads to respiratory distress and lethality in newborn mice. Zfp148 deficiency prevented structural maturation of the prenatal lung without affecting type II cell differentiation or surfactant production. BrdU analyses revealed that Zfp148 deficiency caused proliferation arrest of pulmonary cells at E18.5–19.5. Similarly, Zfp148-deficient fibroblasts exhibited proliferative arrest that was dependent on p53, raising the possibility that cell stress is part of the underlying mechanism. Indeed, Zfp148 deficiency lowered the threshold for activation of p53 under oxidative conditions. Moreover, both in vivo and cellular phenotypes were rescued on Trp53+/− or Trp53−/− backgrounds and by antioxidant treatment. Thus, Zfp148 prevents respiratory distress and lethality in newborn mice by attenuating oxidative stress–dependent p53-activity during the saccular stage of lung development. Our results establish Zfp148 as a novel player in mammalian lung maturation and demonstrate that Zfp148 is critical for cell cycle progression in vivo.

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