Literature DB >> 16201267

Effect of cigarette smoke extract on the proliferation of human airway epithelial cells and expression and activation of FAK.

Li Xu1, Zhenxiang Zhang, Yongjian Xu.   

Abstract

The effect of cigarette smoke extract (CSE) on the proliferation of human airway epithelial cells and the possible mechanism was studied. After airway epithelial cells were treated with different concentrations of CSE for 24 h, the cell proliferation was measured by MTT and the distribution of different cell cycles by flow cytometry. The FAK expression level was detected by Western blot and the degree of tyrosine phosphorylation by immunoprecipitation. The results showed that CSE could inhibit the proliferation of human airway epithelial cells, arrest the epithelial cells in G1 phase of cell cycle, dramatically decrease the number of epithelial cells in S and G2 phases; Meanwhile CSE could decrease the expression level of FAK and the degree of its tyrosine phosphorylation. The above effects of CSE were concentration-dependent. The expression of FAK and the degree of its phosphorylation was positively correlated to the increased number of epithelial cells in G1 phase, and negatively to the number of epithelial cells in S and G2 phases. It was concluded that the mechanism by which CSE could inhibit the proliferation of human epithelial cells was contributed to the increased expression and activation of FAK.

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Year:  2005        PMID: 16201267     DOI: 10.1007/bf02828138

Source DB:  PubMed          Journal:  J Huazhong Univ Sci Technolog Med Sci        ISSN: 1672-0733


  9 in total

1.  Dephosphorylation of focal adhesion kinase (FAK) and loss of focal contacts precede caspase-mediated cleavage of FAK during apoptosis in renal epithelial cells.

Authors:  B van de Water; J F Nagelkerke; J L Stevens
Journal:  J Biol Chem       Date:  1999-05-07       Impact factor: 5.157

2.  Src family kinases are required for integrin-mediated but not for G protein-coupled receptor stimulation of focal adhesion kinase autophosphorylation at Tyr-397.

Authors:  E P Salazar; E Rozengurt
Journal:  J Biol Chem       Date:  2001-02-15       Impact factor: 5.157

3.  Cell migration and proliferation during the in vitro wound repair of the respiratory epithelium.

Authors:  J M Zahm; H Kaplan; A L Hérard; F Doriot; D Pierrot; P Somelette; E Puchelle
Journal:  Cell Motil Cytoskeleton       Date:  1997

4.  Cigarette smoke inhibits lung fibroblast proliferation and chemotaxis.

Authors:  Y Nakamura; D J Romberger; L Tate; R F Ertl; M Kawamoto; Y Adachi; T Mio; J H Sisson; J R Spurzem; S I Rennard
Journal:  Am J Respir Crit Care Med       Date:  1995-05       Impact factor: 21.405

5.  Fibronectin and its alpha 5 beta 1-integrin receptor are involved in the wound-repair process of airway epithelium.

Authors:  A L Hérard; D Pierrot; J Hinnrasky; H Kaplan; D Sheppard; E Puchelle; J M Zahm
Journal:  Am J Physiol       Date:  1996-11

6.  Expression of Fas (CD95) and FasL (CD95L) in human airway epithelium.

Authors:  K J Hamann; D R Dorscheid; F D Ko; A E Conforti; A I Sperling; K F Rabe; S R White
Journal:  Am J Respir Cell Mol Biol       Date:  1998-10       Impact factor: 6.914

7.  Perlecan up-regulation of FRNK suppresses smooth muscle cell proliferation via inhibition of FAK signaling.

Authors:  Heather A Walker; John M Whitelock; Pamela J Garl; Raphael A Nemenoff; Kurt R Stenmark; Mary C M Weiser-Evans
Journal:  Mol Biol Cell       Date:  2003-01-26       Impact factor: 4.138

Review 8.  Focal adhesion kinase: at the crossroads of signal transduction.

Authors:  D Ilić; C H Damsky; T Yamamoto
Journal:  J Cell Sci       Date:  1997-02       Impact factor: 5.285

9.  Mechanism of cigarette smoke condensate-induced acute inflammatory response in human bronchial epithelial cells.

Authors:  Gary R Hellermann; Szilvia B Nagy; Xiaoyuan Kong; Richard F Lockey; Shyam S Mohapatra
Journal:  Respir Res       Date:  2002-07-10
  9 in total

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