Abstract
Background and Aim: A recent transgenic mouse model overexpressing transforming growth factor alpha (TGF-α) led to a phenotype of pulmonary fibrosis. In order to validate this mouse as a model for idiopathic pulmonary fibrosis in humans, we studied the expression of TGF-α in lung tissue of patients with idiopathic pulmonary fibrosis compared to control lung tissue. Methods: Tissue from both groups was obtained from operative specimens and immediately formalin-fixed and paraffin embedded. Contiguous four micron sections were prepared for conventional histochemical staining and staining with antibodies to either TGF-α or the epidermal growth factor-receptor (EGF-R). Immunostaining was performed using the Ventana ES automated immunohistochemistry system. Four cell types were examined (vascular endothelium, bronchial epithelium, type 2 pneumocytes, and fibroblasts) and stain activity was scored on a six point scale. Results: Eleven patients with IPF were compared to seven control subjects. TGF-α immunoreactivity was significantly higher in the IPF patients than in controls in the vascular endothelium, type 2 pneumocytes, and fibroblasts (P < 0.005). [IPF (4(2-4) Median (Range)) than the controls (0.5(0-2), p < 0.0005).] The differences in EGF-R, one of the receptors for TGF-α, between these two patient populations were not as striking. There was a small but significantly greater expression of EGF-R in the bronchial epithelium and type 2 pneumocytes of the IPF patients. Conclusions: TGF-α is overexpressed in patients with IPF, especially in the vascular endothelial cells.
| Original language | English |
|---|---|
| Pages (from-to) | 57-61 |
| Number of pages | 5 |
| Journal | Sarcoidosis Vasculitis and Diffuse Lung Disease |
| Volume | 16 |
| Issue number | 1 |
| State | Published - Mar 1 1999 |
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Keywords
- Epidermal growth factor-receptor
- Idiopathic pulmonary fibrosis
- Transforming growth factor-alpha
ASJC Scopus subject areas
- Pulmonary and Respiratory Medicine
Cite this
Overexpression of transforming growth factor-α and epidermal growth factor-receptor in idiopathic pulmonary fibrosis. / Baughman, Robert P.; Lower, Elyse E.; Miller, Mary Ann; Bejarano, Pablo A.; Heffelfinger, Sue C.
In: Sarcoidosis Vasculitis and Diffuse Lung Disease, Vol. 16, No. 1, 01.03.1999, p. 57-61.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Overexpression of transforming growth factor-α and epidermal growth factor-receptor in idiopathic pulmonary fibrosis
AU - Baughman, Robert P.
AU - Lower, Elyse E.
AU - Miller, Mary Ann
AU - Bejarano, Pablo A.
AU - Heffelfinger, Sue C.
PY - 1999/3/1
Y1 - 1999/3/1
N2 - Background and Aim: A recent transgenic mouse model overexpressing transforming growth factor alpha (TGF-α) led to a phenotype of pulmonary fibrosis. In order to validate this mouse as a model for idiopathic pulmonary fibrosis in humans, we studied the expression of TGF-α in lung tissue of patients with idiopathic pulmonary fibrosis compared to control lung tissue. Methods: Tissue from both groups was obtained from operative specimens and immediately formalin-fixed and paraffin embedded. Contiguous four micron sections were prepared for conventional histochemical staining and staining with antibodies to either TGF-α or the epidermal growth factor-receptor (EGF-R). Immunostaining was performed using the Ventana ES automated immunohistochemistry system. Four cell types were examined (vascular endothelium, bronchial epithelium, type 2 pneumocytes, and fibroblasts) and stain activity was scored on a six point scale. Results: Eleven patients with IPF were compared to seven control subjects. TGF-α immunoreactivity was significantly higher in the IPF patients than in controls in the vascular endothelium, type 2 pneumocytes, and fibroblasts (P < 0.005). [IPF (4(2-4) Median (Range)) than the controls (0.5(0-2), p < 0.0005).] The differences in EGF-R, one of the receptors for TGF-α, between these two patient populations were not as striking. There was a small but significantly greater expression of EGF-R in the bronchial epithelium and type 2 pneumocytes of the IPF patients. Conclusions: TGF-α is overexpressed in patients with IPF, especially in the vascular endothelial cells.
AB - Background and Aim: A recent transgenic mouse model overexpressing transforming growth factor alpha (TGF-α) led to a phenotype of pulmonary fibrosis. In order to validate this mouse as a model for idiopathic pulmonary fibrosis in humans, we studied the expression of TGF-α in lung tissue of patients with idiopathic pulmonary fibrosis compared to control lung tissue. Methods: Tissue from both groups was obtained from operative specimens and immediately formalin-fixed and paraffin embedded. Contiguous four micron sections were prepared for conventional histochemical staining and staining with antibodies to either TGF-α or the epidermal growth factor-receptor (EGF-R). Immunostaining was performed using the Ventana ES automated immunohistochemistry system. Four cell types were examined (vascular endothelium, bronchial epithelium, type 2 pneumocytes, and fibroblasts) and stain activity was scored on a six point scale. Results: Eleven patients with IPF were compared to seven control subjects. TGF-α immunoreactivity was significantly higher in the IPF patients than in controls in the vascular endothelium, type 2 pneumocytes, and fibroblasts (P < 0.005). [IPF (4(2-4) Median (Range)) than the controls (0.5(0-2), p < 0.0005).] The differences in EGF-R, one of the receptors for TGF-α, between these two patient populations were not as striking. There was a small but significantly greater expression of EGF-R in the bronchial epithelium and type 2 pneumocytes of the IPF patients. Conclusions: TGF-α is overexpressed in patients with IPF, especially in the vascular endothelial cells.
KW - Epidermal growth factor-receptor
KW - Idiopathic pulmonary fibrosis
KW - Transforming growth factor-alpha
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UR - http://www.scopus.com/inward/citedby.url?scp=0032910591&partnerID=8YFLogxK
M3 - Article
C2 - 10207942
AN - SCOPUS:0032910591
VL - 16
SP - 57
EP - 61
JO - Sarcoidosis Vasculitis and Diffuse Lung Diseases
JF - Sarcoidosis Vasculitis and Diffuse Lung Diseases
SN - 1124-0490
IS - 1
ER -