scholarly journals Conserved Linkage of Early Growth Response 4, Annexin 4, and Transforming Growth Factor α on Mouse Chromosome 6

Genomics ◽  
1994 ◽  
Vol 19 (2) ◽  
pp. 388-390 ◽  
Author(s):  
Lon L. Barrow ◽  
Karl Simin ◽  
Julie M. Jones ◽  
David C. Lee ◽  
Miriam H. Meisler
Stroke ◽  
2009 ◽  
Vol 40 (2) ◽  
pp. 439-447 ◽  
Author(s):  
Pieter T.G. Bot ◽  
Imo E. Hoefer ◽  
Joost P.G. Sluijter ◽  
Patrick van Vliet ◽  
Anke M. Smits ◽  
...  

2003 ◽  
Vol 279 (8) ◽  
pp. 6883-6892 ◽  
Author(s):  
Seung Joon Baek ◽  
Jong-Sik Kim ◽  
Jennifer B. Nixon ◽  
Richard P. DiAugustine ◽  
Thomas E. Eling

2008 ◽  
Vol 173 (4) ◽  
pp. 1085-1099 ◽  
Author(s):  
Swati Bhattacharyya ◽  
Shu-Jen Chen ◽  
Minghua Wu ◽  
Matthew Warner-Blankenship ◽  
Hongyan Ning ◽  
...  

2013 ◽  
Vol 183 (4) ◽  
pp. 1197-1208 ◽  
Author(s):  
Feng Fang ◽  
Anna J. Shangguan ◽  
Kathleen Kelly ◽  
Jun Wei ◽  
Katherine Gruner ◽  
...  

2004 ◽  
Vol 200 (3) ◽  
pp. 377-389 ◽  
Author(s):  
Chun Geun Lee ◽  
Soo Jung Cho ◽  
Min Jong Kang ◽  
Svetlana P. Chapoval ◽  
Patty J. Lee ◽  
...  

Fibrosis and apoptosis are juxtaposed in pulmonary disorders such as asthma and the interstitial diseases, and transforming growth factor (TGF)-β1 has been implicated in the pathogenesis of these responses. However, the in vivo effector functions of TGF-β1 in the lung and its roles in the pathogenesis of these responses are not completely understood. In addition, the relationships between apoptosis and other TGF-β1–induced responses have not been defined. To address these issues, we targeted bioactive TGF-β1 to the murine lung using a novel externally regulatable, triple transgenic system. TGF-β1 produced a transient wave of epithelial apoptosis that was followed by mononuclear-rich inflammation, tissue fibrosis, myofibroblast and myocyte hyperplasia, and septal rupture with honeycombing. Studies of these mice highlighted the reversibility of this fibrotic response. They also demonstrated that a null mutation of early growth response gene (Egr)-1 or caspase inhibition blocked TGF-β1–induced apoptosis. Interestingly, both interventions markedly ameliorated TGF-β1–induced fibrosis and alveolar remodeling. These studies illustrate the complex effects of TGF-β1 in vivo and define the critical role of Egr-1 in the TGF-β1 phenotype. They also demonstrate that Egr-1–mediated apoptosis is a prerequisite for TGF-β1–induced fibrosis and remodeling.


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