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Figure 5.: Histological assessment of lung fibrosis. (A) Photomicrographs of hematoxylin and eosin–stained lung tissue sections from control mice, irradiated mice (20 Gy, RT), and mice treated with SU9518 after thoracic irradiation (intervention, RT+SU9518) at 12, 16, 20, and 24 wk after radiation. Bar, 100 μm. (B) Masson's trichrome staining of lung sections 12, 16, 20, and 24 wk after irradiation without (RT) or with administration of SU9518 (RT+SU9518). Examples of focal fibrotic lesions (*), areas of “normal” lung (black arrows), and inflammatory cell infiltration (L, red) are marked. Scale bar, 100 μm. (C) Time course of septal edema development in irradiated mice (RT) with maximum edema at 72 h after radiation (P < 0.05 RT vs. control for each time from 0 h to 4 wk). The preventive or interventive administration of SU9518 (SU9518+RT, RT+SU9518) had significant suppressive effects on edema development, except at 72 h after radiation (P < 0.05 vs. RT). (D) Septal fibrosis develops progressively several weeks after radiation (P < 0.05 RT vs. control for each time point after week 2). Both the SU9518 intervention (RT+SU9518) and prevention (SU9518+RT) treatment significantly reduced the progression of septal fibrosis, as measured by the extent of alveolar wall thickness, at all time points after week 2 (P < 0.05 vs. RT for each time point). However, septal fibrosis was not completely inhibited by the compound (P < 0.05 vs. the control after week 2). (E) Quantitative analysis of leukocyte numbers at various times after irradiation (20 Gy, RT) reveals two peaks. SU9518 before (SU9518+RT) or after (RT+SU9518) irradiation did not significantly attenuate the early leukocyte peak (P > 0.2). Both the preventive (SU9518+RT) and interventional (RT+SU9518) administration of SU9518 significantly inhibited the fibrosis-associated second inflammatory response during weeks 2–26 (P < 0.05 vs. RT for each time point). However, the second fibrosis-associated inflammation was not completely inhibited by SU9518 (P < 0.05 vs. the control after week 2). Bars are mean ± SD.

Image Text (High Precision): Control Fibrosis Septal Time edema radiotherapy

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Abstract

Pulmonary fibrosis is the consequence of a variety of diseases with no satisfying treatment option. Therapy-induced fibrosis also limits the efficacy of chemotherapy and radiotherapy in numerous cancers. Here, we studied the potential of platelet-derived growth factor (PDGF) receptor tyrosine kinase inhibitors (RTKIs) to attenuate radiation-induced pulmonary fibrosis. Thoraces of C57BL/6 mice were irradiated (20 Gy), and mice were treated with three distinct PDGF RTKIs (SU9518, SU11657, or Imatinib). Irradiation was found to induce severe lung fibrosis resulting in dramatically reduced mouse survival. Treatment with PDGF RTKIs markedly attenuated the development of pulmonary fibrosis in excellent correlation with clinical, histological, and computed tomography results. Importantly, RTKIs also prolonged the life span of irradiated mice. We found that radiation up-regulated expression of PDGF (A–D) isoforms leading to phosphorylation of PDGF receptor, which was strongly inhibited by RTKIs. Our findings suggest a pivotal role of PDGF signaling in the pathogenesis of pulmonary fibrosis and indicate that inhibition of fibrogenesis, rather than inflammation, is critical to antifibrotic treatment. This study points the way to a potential new approach for treating idiopathic or therapy-related forms of lung fibrosis.


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