Attenuation of p38α MAPK stress response signaling delays the <i>in vivo</i> aging of skeletal muscle myofibers and progenitor cells

John Papaconstantinou; Chen Z. Wang; Min Zhang; San Yang; James Deford; Dmitry V. Bulavin; Naseem H. Ansari

doi:doi:10.18632/aging.100802

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Research Paper Volume 7, Issue 9 pp 718—733

Attenuation of p38α MAPK stress response signaling delays the in vivo aging of skeletal muscle myofibers and progenitor cells

Figure 8. Expression of the p16^Ink4a tumor suppressor gene by the gastrocnemius of young (2 mos), middle aged (13.5 mos) and aged (20 mos) WT and DN-p38α^AF/+ mice. (A: upper panel) The levels of expression of the p16^Ink4a gene are significantly higher throughout the lifespan of WT mice compared to corresponding age matched DN-p38α^AF/+ mice. Data for WT mice are depicted in (A1) young (2.0 mos); (A3) middle aged (13.5 mos); (A5) aged (20 mos); (A: lower panel) Data for DN-p38α^AF/+ mice are depicted in (A2) young (2 mos); (A4) middle aged (13.5 mos) and aged (A6) aged (20 mos). (B) Bar graph presentation of the Western blot analyses of (C). *p = 0.05 vs. WT of the same age. (C) Western blot analyses of the level of expression of p16^Ink4a in gastrocnemius of young (2 mos); middle aged (13.5 mos) and aged (20 mos) WT and DN-p38α^AF/+ mice.