scholarly journals Selection of rhinovirus 1A variants adapted for growth in mouse lung epithelial cells

Virology ◽  
2011 ◽  
Vol 420 (2) ◽  
pp. 82-88 ◽  
Author(s):  
Angela L. Rasmussen ◽  
Vincent R. Racaniello
Author(s):  
Jin-Soo Park ◽  
RyeonJin Cho ◽  
Eun-Young Kang ◽  
Yeon-Mok Oh

AbstractEmphysema, a pathological component of chronic obstructive pulmonary disease, causes irreversible damage to the lung. Previous studies have shown that Slit plays essential roles in cell proliferation, angiogenesis, and organ development. In this study, we evaluated the effect of Slit2 on the proliferation and migration of mouse lung epithelial cells and its role in regeneration in an emphysema lung mouse model. Here, we have shown that Slit2/Robo signaling contributes to the regeneration of lungs damaged by emphysema. Mouse epithelial lung cells treated with Slit2 exhibited increased proliferation and migration in vitro. Our results also showed that Slit2 administration improved alveolar regeneration in the emphysema mouse model in vivo. Furthermore, Slit2/Robo signaling increased the phosphorylation of ERK and Akt, which was mediated by Ras activity. These Slit2-mediated cellular signaling processes may be involved in the proliferation and migration of mouse lung epithelial cells and are also associated with the potential mechanism of lung regeneration. Our findings suggest that Slit2 administration may be beneficial for alveolar regeneration in lungs damaged by emphysema.


Author(s):  
Taku Sato ◽  
Mami Morita ◽  
Ryota Tanaka ◽  
Yui Inoue ◽  
Miyuki Nomura ◽  
...  

2015 ◽  
Vol 10 (12) ◽  
pp. 2891-2899 ◽  
Author(s):  
Jaya M. Matharage ◽  
John D. Minna ◽  
Rolf A. Brekken ◽  
D. Gomika Udugamasooriya

2006 ◽  
Vol 8 (9-10) ◽  
pp. 1447-1459 ◽  
Author(s):  
Priya Ranjan ◽  
Vikas Anathy ◽  
Peter M. Burch ◽  
Kelly Weirather ◽  
J. David Lambeth ◽  
...  

2021 ◽  
Author(s):  
Chin Chiahsuan ◽  
John Lee ◽  
Ranjith Ravichandran ◽  
Timothy Fleming ◽  
Stephen Wheatcroft ◽  
...  

AbstractAccumulation of senescent cells contributes to age related diseases including idiopathic pulmonary fibrosis (IPF). Insulin-like growth factor binding proteins (IGFBPs) are evolutionarily conserved proteins that play a vital role in many biological processes. Overall, little is known about the functions of IGFBP2 in the epigenetic regulation of cellular senescence and pulmonary fibrosis. Here, we show that Igfbp2 expression was significantly downregulated at both mRNA and protein levels in a low-dose bleomycin-induced pulmonary fibrosis model of aged mice. Using the reduced representation of bisulfite sequencing technique, we demonstrated Igfbp2 downregulation is attributed to DNA methylation of CpG islands in fibrotic lungs of aged mice. Furthermore, Igfbp2 siRNA knockdown increased both P53 and P21 protein levels in mouse lung epithelial cells exposed to hypoxia treatment. Lentiviral mediated expression of Igfb2 decreased P21 protein levels and significantly reduced beta galactosidase activity in mouse lung epithelial cells challenged with a senescent drug (atazanavir) and hypoxia treatments. Using the RT2 Profiler PCR Array, we found that P21, PAI-1, IRF-5 and IRF-7, important regulators of senescence pathway, were significantly downregulated specifically in type-II alveolar epithelial cells (AECs) of aged human-Igfbp2 transgenic mice after bleomycin challenge. Finally, transgenic expression of human-Igfbp2 in type-II AECs from aged bleomycin challenged mice significantly decreased senescent associated secretory phenotype factors and also reduced extracellular matrix markers compared to aged wild-type mice challenged with bleomycin injury. Collectively, these findings reveal that epigenetic repression of Igfbp2 promotes pulmonary fibrosis and that restoring IGFBP2 in fibrotic lungs could prove effective in IPF treatment.


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