Inhibition of Bcl-2/xl With ABT-263 Selectively Kills Senescent Type II Pneumocytes and Reverses Persistent Pulmonary Fibrosis Induced by Ionizing Radiation in Mice

Int J Radiat Oncol Biol Phys. 2017 Oct 1;99(2):353-361. doi: 10.1016/j.ijrobp.2017.02.216. Epub 2017 Mar 4.

Abstract

Purpose: Ionizing radiation (IR)-induced pulmonary fibrosis (PF) is an irreversible and severe late effect of thoracic radiation therapy. The goal of this study was to determine whether clearance of senescent cells with ABT-263, a senolytic drug that can selectively kill senescent cells, can reverse PF.

Methods and materials: C57BL/6J mice were exposed to a single dose of 17 Gy on the right side of the thorax. Sixteen weeks after IR, they were treated with 2 cycles of vehicle or ABT-263 (50 mg/kg per day for 5 days per cycle) by gavage. The effects of ABT-263 on IR-induced increases in senescent cells; elevation in the expression of selective inflammatory cytokines, matrix metalloproteinases, and tissue inhibitors of matrix metalloproteinases; and the severity of the tissue injury and fibrosis in the irradiated lungs were evaluated 3 weeks after the last treatment, in comparison with the changes observed in the irradiated lungs before treatment or after vehicle treatment.

Results: At 16 weeks after exposure of C57BL/6 mice to a single dose of 17 Gy, thoracic irradiation resulted in persistent PF associated with a significant increase in senescent cells. Treatment of the irradiated mice with ABT-263 after persistent PF had developed reduced senescent cells and reversed the disease.

Conclusions: To our knowledge, this is the first study to demonstrate that PF can be reversed by a senolytic drug such as ABT-263 after it becomes a progressive disease. Therefore, ABT-263 has the potential to be developed as a new treatment for PF.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, N.I.H., Extramural
  • Research Support, N.I.H., Intramural

MeSH terms

  • Alveolar Epithelial Cells / drug effects*
  • Alveolar Epithelial Cells / pathology
  • Aniline Compounds / therapeutic use*
  • Animals
  • Antineoplastic Agents / administration & dosage
  • Antineoplastic Agents / therapeutic use*
  • Cellular Senescence*
  • Cyclin-Dependent Kinase Inhibitor p16 / analysis
  • Cyclin-Dependent Kinase Inhibitor p16 / genetics
  • Cytokines / analysis
  • Hydroxyproline / analysis
  • Inflammation Mediators / metabolism
  • Lung / chemistry
  • Lung / enzymology
  • Lung / radiation effects
  • Male
  • Mice
  • Mice, Inbred C57BL
  • Polymerase Chain Reaction
  • Proto-Oncogene Proteins c-bcl-2 / analysis
  • Proto-Oncogene Proteins c-bcl-2 / genetics
  • RNA, Messenger / analysis
  • Radiation Pneumonitis / drug therapy*
  • Radiation Pneumonitis / genetics
  • Radiation Pneumonitis / pathology
  • Radiation, Ionizing
  • Sulfonamides / therapeutic use*
  • bcl-2-Associated X Protein / antagonists & inhibitors*
  • bcl-2-Associated X Protein / metabolism
  • beta-Galactosidase / analysis

Substances

  • Aniline Compounds
  • Antineoplastic Agents
  • Cdkn2a protein, mouse
  • Cyclin-Dependent Kinase Inhibitor p16
  • Cytokines
  • Inflammation Mediators
  • Proto-Oncogene Proteins c-bcl-2
  • RNA, Messenger
  • Sulfonamides
  • bcl-2-Associated X Protein
  • beta-Galactosidase
  • Hydroxyproline
  • navitoclax