| First Author | Chen Z | Year | 2019 |
| Journal | Int J Radiat Oncol Biol Phys | Volume | 103 |
| Issue | 1 | Pages | 208-216 |
| PubMed ID | 30171878 | Mgi Jnum | J:318763 |
| Mgi Id | MGI:6859983 | Doi | 10.1016/j.ijrobp.2018.08.035 |
| Citation | Chen Z, et al. (2019) Haplodeletion of Follistatin-Like 1 Attenuates Radiation-Induced Pulmonary Fibrosis in Mice. Int J Radiat Oncol Biol Phys 103(1):208-216 |
| abstractText | PURPOSE: Radiation-induced pulmonary fibrosis (RIPF) is a severe and life-threatening complication of radiation therapy in patients with thoracic cancer; however, the exact molecular mechanisms remain unknown, and there is no effective treatment method in clinic. Here, we assessed the role of follistatin-like 1 (Fstl1) in RIPF. METHODS AND MATERIALS: Protein and messenger RNA levels of Fstl1 in lung tissues from symptomatic RIPF patients, Rhesus macaques, and mice were assessed. Fibrotic and inflammatory responses to radiation-induced lung injury and accumulation of myofibroblasts in Fstl1 haplodeficient (Fstl1(+/-)) mice were determined. Finally, radiation-induced differentiation and activation of fibroblasts in primary Fstl1(+/-) lung fibroblasts were evaluated. RESULTS: FSTL1 amounts were significantly increased in serum and/or radiation-injured lung specimens from symptomatic RIPF patients, Rhesus macaques, and mice. Haplodeletion of Fstl1 in Fstl1(+/-) mice was protective against x-ray-induced lung injury in mice in vivo, as well as myofibroblast activation in vitro. CONCLUSIONS: These findings suggest that Fstl1 plays an important role in lung fibrosis and may offer a potential approach to attenuate RIPF in radiation therapy of patients with thoracic cancer. |
