Ionizing Radiation Causes a Dose-Dependent Release of Transforming Growth Factor α In vitro from Irradiated Xenografts and during Palliative Treatment of Hormone-Refractory Prostate Carcinoma

2004 ◽  
Vol 10 (17) ◽  
pp. 5724-5731 ◽  
Author(s):  
Michael Hagan ◽  
Adly Yacoub ◽  
Paul Dent
Keyword(s):  
Growth Factor ◽  
Ionizing Radiation ◽  
Prostate Carcinoma ◽  
Palliative Treatment ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Α ◽  
Hormone Refractory ◽  
Factor Α ◽  
Dose Dependent

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.

Transforming growth factor-α directly augments histidine decarboxylase and vesicular monoamine transporter 2 production in rat enterochromaffin-like cells

2004 ◽  
Vol 286 (3) ◽  
pp. G508-G514 ◽  
Author(s):  
Hideaki Kazumori ◽  
Shunji Ishihara ◽  
Mohammad A. K. Rumi ◽  
Cesar F. Ortega-Cava ◽  
Yasunori Kadowaki ◽  
...  
Keyword(s):  
Growth Factor ◽  
Transforming Growth Factor ◽  
Histidine Decarboxylase ◽  
Vesicular Monoamine Transporter ◽  
Vesicular Monoamine Transporter 2 ◽  
Transforming Growth Factor Α ◽  
Ecl Cells ◽  
Factor Α

For the production and vesicle storage of histamine, Enterochromaffin-like (ECL) cells express histidine decarboxylase (HDC) and vesicular monoamine transporter 2 (VMAT2). Although HDC and VMAT2 show dynamic changes during gastric ulcer healing, the control system of their expression has not been fully investigated. In the present study, we investigated the effect of transforming growth factor-α (TGF-α) and proinflammatory cytokines on HDC and VMAT2 expression in rat ECL cells. Time course changes in the expression of TGF-α during the healing of acetic acid-induced ulcers were studied. EGF receptor (EGFR) expression was also examined in ECL cells, whereas the direct effects of TGF-α and proinflammatory cytokines on HDC and VMAT2 expression in ECL cells were investigated using in vivo and in vitro models. During the process of ulcer healing, expression of TGF-α mRNA was markedly augmented. Furthermore, EGFR was identified in isolated ECL cells. TGF-α stimulated HDC and VMAT2 mRNA expression and protein production and also increased histamine release from ECL cells. Selective EGFR tyrosine kinase inhibitor tyrphostin AG1478 almost completely inhibited HDC and VMAT2 gene expression induced by TGF-α in vivo and in vitro. During gastric mucosal injury, TGF-α was found to stimulate ECL cell functions by increasing HDC and VMAT2 expression.

Interleukin-1β augments in vitro alveolar epithelial repair

2000 ◽  
Vol 279 (6) ◽  
pp. L1184-L1190 ◽  
Author(s):  
Thomas Geiser ◽  
Pierre-Henri Jarreau ◽  
Kamran Atabai ◽  
Michael A. Matthay
Keyword(s):  
Acute Lung Injury ◽  
Growth Factor ◽  
Lung Injury ◽  
Wound Repair ◽  
Transforming Growth Factor ◽  
Epithelial Repair ◽  
Transforming Growth Factor Α ◽  
Alveolar Epithelial ◽  
Factor Α

Biologically active interleukin (IL)-1β is present in the pulmonary edema fluid obtained from patients with acute lung injury and has been implicated as an important early mediator of nonpulmonary epithelial wound repair. Therefore, we tested the hypothesis that IL-1β would enhance wound repair in cultured monolayers from rat alveolar epithelial type II cells. IL-1β (20 ng/ml) increased the rate of in vitro alveolar epithelial repair by 118 ± 11% compared with that in serum-free medium control cells ( P < 0.01). IL-1β induced cell spreading and migration at the edge of the wound but not proliferation. Neutralizing antibodies to epidermal growth factor (EGF) and transforming growth factor-α or inhibition of the EGF receptor by tyrphostin AG-1478 or genistein inhibited IL-1β-induced alveolar epithelial repair, indicating that IL-1β enhances in vitro alveolar epithelial repair by an EGF- or transforming growth factor-α-dependent mechanism. Moreover, the mitogen-activated protein kinase pathway is involved in IL-1β-induced alveolar epithelial repair because inhibition of extracellular signal-regulated kinase activation by PD-98059 inhibited IL-1β-induced alveolar epithelial repair. In conclusion, IL-1β augments in vitro alveolar epithelial repair, indicating a possible novel role for IL-1β in the early repair process of the alveolar epithelium in acute lung injury.

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