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. 2012 Nov 13;21(2):456–465. doi: 10.1038/mt.2012.183

Figure 1.

Figure 1

Radiation-induced lung injury (RILI) was associated with transforming growth factor-β1 (TGF-β1) expression. (a) The time course of active TGF-β1 levels in the bronchoalveolar lavage fluid (BALF) (upper panel) and plasma (lower panel) after thoracic irradiation, as measured by enzyme-linked immunosorbent assay (ELISA) (*P < 0.05, **P < 0.01, n = 6). (b) Schematic representation of action of sTβR. The active TGF-β1 initially binds to the extracellular domain of TGF-β type II receptor (Ex-TβRII), recruits and phosphorylates the type I receptor to form heteromeric complexes, thus triggering the subsequent activation of downstream signal transduction. sTβR competes with TβRII to bind with active TGF-β1, subsequently blocking the effects of TGF-β1, which plays a crucial role in collagen deposition and fibrosis. (c) Adenovirus construction. PCR products of Ex-TβRII, IgG1 Fc, and fusion gene sTβR were detected by agarose gel electrophoresis. (d) Western blot analysis of sTβR protein in 293 cells 48 hours after Ad-sTβR, Ad-null transduction. (e) The sTβR levels in BALF were assayed by ELISA after administrations of phosphate-buffered saline (PBS), Ad-null (1.25 × 108 PFU), Ad-sTβR (1.25 × 108 PFU), mesenchymal stem cells (MSCs) (5 × 105), and Ad-sTβR-MSCs (1.25 × 108 PFU, 5 × 105 cells) (*P < 0.05, **P < 0.01, Ad-sTβR-MSCs versus Ad-sTβR; n = 6).