scholarly journals In Vivo Activation of Rat Aortic Platelet-Derived Growth Factor and Epidermal Growth Factor Receptors by Angiotensin II and Hypertension

2000 ◽  
Vol 20 (12) ◽  
pp. 2539-2545 ◽  
Author(s):  
Shokei Kim ◽  
Yumei Zhan ◽  
Yasukatsu Izumi ◽  
Hideo Yasumoto ◽  
Masahiko Yano ◽  
...  
Apmis ◽  
2008 ◽  
Vol 116 (5) ◽  
pp. 432-433
Author(s):  
Marie-Thérése Stockhausen ◽  
Mette Villingshøj ◽  
Mogens Spang-Thomsen ◽  
Helle Broholm ◽  
Michael Kosteljanetz ◽  
...  

2001 ◽  
Vol 280 (1) ◽  
pp. L165-L172 ◽  
Author(s):  
Kiyoshi Takeyama ◽  
Birgit Jung ◽  
Jae Jeong Shim ◽  
Pierre-Regis Burgel ◽  
Trang Dao-Pick ◽  
...  

Mucus hypersecretion from hyperplastic airway goblet cells is a hallmark of chronic obstructive pulmonary disease (COPD). Although cigarette smoking is thought to be involved in mucus hypersecretion in COPD, the mechanism by which cigarette smoke induces mucus overproduction is unknown. Here we show that activation of epidermal growth factor receptors (EGFR) is responsible for mucin production after inhalation of cigarette smoke in airways in vitro and in vivo. In the airway epithelial cell line NCI-H292, exposure to cigarette smoke upregulated the EGFR mRNA expression and induced activation of EGFR-specific tyrosine phosphorylation, resulting in upregulation of MUC5AC mRNA and protein production, effects that were inhibited completely by selective EGFR tyrosine kinase inhibitors (BIBX1522, AG-1478) and that were decreased by antioxidants. In vivo, cigarette smoke inhalation increased MUC5AC mRNA and goblet cell production in rat airways, effects that were prevented by pretreatment with BIBX1522. These effects may explain the goblet cell hyperplasia that occurs in COPD and may provide a novel strategy for therapy in airway hypersecretory diseases.


2002 ◽  
Vol 20 (4) ◽  
pp. 693-699 ◽  
Author(s):  
Paola De Paolis ◽  
Antonio Porcellini ◽  
Carmine Savoia ◽  
Alessia Lombardi ◽  
Bruna Gigante ◽  
...  

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