ATM is a key driver of NF-κB-dependent DNA-damage-induced senescence, stem cell dysfunction and aging

Jing Zhao; Lei Zhang; Aiping Lu; Yingchao Han; Debora Colangelo; Christina Bukata; Alex Scibetta; Matthew J. Yousefzadeh; Xuesen Li; Aditi U. Gurkar; Sara J. McGowan; Luise Angelini; Ryan O’Kelly; Hongshuai Li; Lana Corbo; Tokio Sano; Heather Nick; Enrico Pola; Smitha P.S. Pilla; Warren C. Ladiges; Nam Vo; Johnny Huard; Laura J. Niedernhofer; Paul D. Robbins

doi:doi:10.18632/aging.102863

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Priority Research Paper Volume 12, Issue 6 pp 4688—4710

ATM is a key driver of NF-κB-dependent DNA-damage-induced senescence, stem cell dysfunction and aging

Figure 6. Genetic reduction of Atm improves bone and intervertebral disc pathology in progeroid Ercc1^-/Δ mice. (A) Representative micro-CT images of lumber spines comparing severity of osteoporosis in 16-week-old WT, Ercc1^-/Δ, Ercc1^-/ΔAtm^+/- mice. n=3-5 per group. Quantification of vertebral porosity, trabecular number, trabecular separation, thickness of trabecular bone was performed and shown. (B) Safranin O staining for disc matrix in thoracic discs from 12-week-old Ercc1^-/Δ and Ercc1^-/ΔAtm^+/- mice. (C) GAG content measured by DMMB assays with NP tissues isolated from 12-week-old lumber discs. n=3 each group. Mean+/- s.e.m. P value was determined using Student’s t-test. **p<0.01.