Changes of apoptosis-related proteins in hippocampus of SAM mouse in development and aging

• Published in: Neurobiology of aging Vol. 27; no. 5; pp. 782.e1 - 782.e10
• Main Authors: Wu, Yan, Zhang, Ai-Qun, Wai, Maria S.M., Lai, Helen W.L., Wu, Sheng-Xi, Yew, David T.
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 01.05.2006
• Subjects: Aging; Aging - genetics; Aging - metabolism; Animals; Apoptosis; Apoptosis - physiology; Bcl-2 family; Benzoxazines; Blotting, Western; Caspases; Caspases - biosynthesis; Caspases - genetics; Coloring Agents; Data Interpretation, Statistical; Female; Hippocampus - metabolism; Histocytochemistry; In Situ Nick-End Labeling; Learning Disorders - genetics; Learning Disorders - metabolism; Memory Disorders - genetics; Memory Disorders - metabolism; Mice; Microscopy, Electron, Transmission; Nerve Tissue Proteins - physiology; Oxazines; Pregnancy; Proto-Oncogene Proteins c-bcl-2 - biosynthesis; Proto-Oncogene Proteins c-bcl-2 - genetics; Pyramidal Cells - metabolism; Pyramidal Cells - ultrastructure; SAM; DTT; G; HRP; CNS; TUNEL; SAMR; SLM; SAMP; Aging; mit; Lf; SO; Nuc; SP; SR; SDS; DAB; ER; Bcl-2 family; PB; r; Caspases; TEM; SAM; Apoptosis
• ISSN: 0197-4580; 1558-1497
• DOI: 10.1016/j.neurobiolaging.2005.07.014

Expression of Caspase and Bcl-2 proteins was examined in the hippocampus of senescence-accelerated mice (SAM, P8 and R1 strain) from E19 to 16 months of age. Immunoblotting analysis showed no upregulation of pro-apoptotic proteins (caspase-2L, -3, -6, -8, -9, and Bax) with age while all the anti-apoptotic proteins (caspase-2S, Bcl-2, and Bcl-XL) remained unchanged during aging. Terminal dUTP nick end labeling (TUNEL) and electron microscopy on the hippocampus of 3- and 16-month-old SAM revealed very few TUNEL positive cells in both groups. Morphometric study further showed neuronal loss in the hippocampus was not age-related. Our results suggest apoptosis and cell loss are minor events in the hippocampus of SAM mice and are unlikely to be the cause of functional decline during aging in SAM.