Horizontal basal cell proliferation in the olfactory epithelium of transforming growth factor-α transgenic mice

2000 ◽  
Vol 299 (2) ◽  
pp. 185-192
Author(s):  
Thomas V. Getchell ◽  
Rama Krishna Narla ◽  
Susan Little ◽  
James F. Hyde ◽  
Marilyn L. Getchell
Keyword(s):  
Cell Proliferation ◽  
Growth Factor ◽  
Transgenic Mice ◽  
Olfactory Epithelium ◽  
Basal Cell ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Α ◽  
Factor Α

Horizontal basal cell proliferation in the olfactory epithelium of transforming growth factor-α transgenic mice

1999 ◽  
Vol 299 (2) ◽  
pp. 185-192
Author(s):  
Thomas V. Getchell ◽  
Rama Krishna Narla ◽  
Susan Little ◽  
James F. Hyde ◽  
Marilyn L. Getchell
Keyword(s):  
Cell Proliferation ◽  
Growth Factor ◽  
Transgenic Mice ◽  
Olfactory Epithelium ◽  
Basal Cell ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Α ◽  
Factor Α

scholarly journals Mammary Carcinogenesis Is Preceded by Altered Epithelial Cell Turnover in Transforming Growth Factor-α and c-myc Transgenic Mice

2006 ◽  
Vol 169 (5) ◽  
pp. 1821-1832 ◽  
Author(s):  
Teresa A. Rose-Hellekant ◽  
Kristin M. Wentworth ◽  
Sarah Nikolai ◽  
Donald W. Kundel ◽  
Eric P. Sandgren
Keyword(s):  
Growth Factor ◽  
Epithelial Cell ◽  
Transgenic Mice ◽  
Transforming Growth Factor ◽  
Mammary Carcinogenesis ◽  
Cell Turnover ◽  
Transforming Growth Factor Α ◽  
Factor Α

Dose-dependent lung remodeling in transgenic mice expressing transforming growth factor-α

2001 ◽  
Vol 281 (5) ◽  
pp. L1088-L1094 ◽  
Author(s):  
William D. Hardie ◽  
Alyssa Piljan-Gentle ◽  
Michelle R. Dunlavy ◽  
Machiko Ikegami ◽  
Thomas R. Korfhagen
Keyword(s):  
Growth Factor ◽  
Transgenic Mice ◽  
Transforming Growth Factor ◽  
Lavage Fluid ◽  
Proliferating Cells ◽  
Transforming Growth Factor Α ◽  
Lung Remodeling ◽  
Transgenic Lines ◽  
Factor Α ◽  
Dose Dependent

Transgenic mice overexpressing human transforming growth factor-α (TGF-α) develop emphysema and fibrosis during postnatal alveologenesis. To assess dose-related pulmonary alterations, four distinct transgenic lines expressing different amounts of TGF-α in the distal lung under control of the surfactant protein C (SP-C) promoter were characterized. Mean lung homogenate TGF-α levels ranged from 388 ± 40 pg/ml in the lowest expressing line to 1,247 ± 33 pg/ml in the highest expressing line. Histological assessment demonstrated progressive alveolar airspace size changes that were more severe in the higher expressing TGF-α lines. Pleural and parenchymal fibrosis were only detected in the highest expressing line ( line 28), and increasing terminal airspace area was associated with increasing TGF-α expression. Hysteresis on pressure-volume curves was significantly reduced in line 28 mice compared with other lines of mice. There were no differences in bronchoalveolar lavage fluid cell count or differential that would indicate any evidence of lung inflammation among all transgenic lines. Proliferating cells were increased in line 28 without alterations of numbers of type II cells. We conclude that TGF-α lung remodeling in transgenic mice is dose dependent and is independent of pulmonary inflammation.

scholarly journals Interactive Effects of c-myc and Transforming Growth Factor α Transgenes on Liver Tumor Development in Simian Virus 40 T Antigen Transgenic Mice

1998 ◽  
Vol 35 (4) ◽  
pp. 283-291 ◽  
Author(s):  
A. Enomoto ◽  
E. P. Sandgren ◽  
R. R. Maronpot
Keyword(s):  
Cell Proliferation ◽  
Growth Factor ◽  
Transforming Growth Factor ◽  
Liver Tumors ◽  
Simian Virus 40 ◽  
Simian Virus ◽  
T Antigen ◽  
Transforming Growth Factor Α ◽  
Neoplastic Lesions ◽  
Factor Α

To analyze the effects of c- myc and transforming growth factor α (TGFα) on hepatocarcinogenesis induced by simian virus 40 T antigen (TAg), livers from single and bitransgenic mice, 3 to 11 mice per line, were examined morphologically 1 to 8 weeks after birth. Mice carrying c- myc or TGFα alone exhibited centrilobular hypertrophy and increased apoptosis (c- myc mice only) of hepatocytes after 3 or 4 weeks of age, but no detectable changes in cell proliferation or proliferative lesions were observed in either line during the 8 weeks. Mice carrying TAg alone exhibited increased cell proliferation, apoptosis, and dysplasia of hepatocytes with notably high mitotic and apoptotic indices as major changes before development of putative preneoplastic lesions after 4 weeks of age and neoplastic lesions after 6 weeks. In bitransgenic mice coexpressing c- myc or TGFα with TAg, nonproliferative lesions and mitotic and apoptotic indices were similar to those in mice carrying TAg alone. In TAg X c- myc bitransgenic mice, however, both preneoplastic and neoplastic lesions developed sooner and grew more rapidly than those in TAg mice, whereas in TAg X TGFα bitransgenic mice, rapid tumor growth was the principle observation. Because of the effects of transgene coexpression, livers from TAg X c- myc and TAg X TGFα mice had multiple tumors as early as 3 and 6 weeks of age, respectively. The results indicate cooperative functions of c- myc and TGFα with TAg during development and/or growth of liver tumors in vivo.

Dose-Related Protection from Nickel-Induced Lung Injury in Transgenic Mice Expressing Human Transforming Growth Factor- α

2002 ◽  
Vol 26 (4) ◽  
pp. 430-437 ◽  
Author(s):  
William D. Hardie ◽  
Daniel R. Prows ◽  
Alyssa Piljan-Gentle ◽  
Michelle R. Dunlavy ◽  
Scott C. Wesselkamper ◽  
...  
Keyword(s):  
Growth Factor ◽  
Lung Injury ◽  
Transgenic Mice ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Α ◽  
Factor Α
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