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Aβ25-35 Suppresses Mitochondrial Biogenesis in Primary Hippocampal Neurons.
Cell Mol Neurobiol. 2016 Jan; 36(1):83-91.CM

Abstract

Mitochondrial biogenesis is involved in the regulation of mitochondrial content, morphology, and function. Impaired mitochondrial biogenesis has been observed in Alzheimer's disease. Amyloid-β (Aβ) has been shown to cause mitochondrial dysfunction in cultured neurons, but its role in mitochondrial biogenesis in neurons remains poorly defined. AMP-activated protein kinase (AMPK) and sirtuin 1 (SIRT1) are key energy-sensing molecules regulating mitochondrial biogenesis. In addition, peroxisome proliferator-activated receptor-γ coactivator 1-alpha (PGC-1α), the master regulator of mitochondrial biogenesis, is a target for SIRT1 deacetylase activity. In this study, we investigated the effects of Aβ25-35 on mitochondrial biogenesis in cultured hippocampal neurons and the underlying mechanisms. In primary hippocampal neurons, we found that 24-h incubation with Aβ25-35 suppressed both phosphorylations of AMPK and SIRT1 expression and increased PGC-1α acetylation expression. In addition, Aβ25-35 also resulted in a decrease in mitochondrial DNA copy number, as well as decreases in the expression of mitochondrial biogenesis factors (PGC-1α, NRF 1, NRF 2, and Tfam). Taken together, these data show that Aβ25-35 suppresses mitochondrial biogenesis in hippocampal neurons. Aβ25-35-induced impairment of mitochondrial biogenesis may be associated with the inhibition of the AMPK-SIRT1-PGC-1α pathway.

Authors+Show Affiliations

Department of Integrated Traditional Chinese and Western Medicine, Fujian University of Traditional Chinese Medicine, Fuzhou, 350122, Fujian, People's Republic of China. fjdwg601@163.com.Department of Integrated Traditional Chinese and Western Medicine, Fujian University of Traditional Chinese Medicine, Fuzhou, 350122, Fujian, People's Republic of China.The Third People's Hospital of Fujian Province, Fuzhou, 350122, Fujian, People's Republic of China.Department of Integrated Traditional Chinese and Western Medicine, Fujian University of Traditional Chinese Medicine, Fuzhou, 350122, Fujian, People's Republic of China.Department of Integrated Traditional Chinese and Western Medicine, Fujian University of Traditional Chinese Medicine, Fuzhou, 350122, Fujian, People's Republic of China.Department of Integrated Traditional Chinese and Western Medicine, Fujian University of Traditional Chinese Medicine, Fuzhou, 350122, Fujian, People's Republic of China.Department of Integrated Traditional Chinese and Western Medicine, Fujian University of Traditional Chinese Medicine, Fuzhou, 350122, Fujian, People's Republic of China.

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

26055049

Citation

Dong, Weiguo, et al. "Aβ25-35 Suppresses Mitochondrial Biogenesis in Primary Hippocampal Neurons." Cellular and Molecular Neurobiology, vol. 36, no. 1, 2016, pp. 83-91.
Dong W, Wang F, Guo W, et al. Aβ25-35 Suppresses Mitochondrial Biogenesis in Primary Hippocampal Neurons. Cell Mol Neurobiol. 2016;36(1):83-91.
Dong, W., Wang, F., Guo, W., Zheng, X., Chen, Y., Zhang, W., & Shi, H. (2016). Aβ25-35 Suppresses Mitochondrial Biogenesis in Primary Hippocampal Neurons. Cellular and Molecular Neurobiology, 36(1), 83-91. https://doi.org/10.1007/s10571-015-0222-6
Dong W, et al. Aβ25-35 Suppresses Mitochondrial Biogenesis in Primary Hippocampal Neurons. Cell Mol Neurobiol. 2016;36(1):83-91. PubMed PMID: 26055049.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Aβ25-35 Suppresses Mitochondrial Biogenesis in Primary Hippocampal Neurons. AU - Dong,Weiguo, AU - Wang,Feng, AU - Guo,Wanqing, AU - Zheng,Xuehua, AU - Chen,Yue, AU - Zhang,Wenguang, AU - Shi,Hong, Y1 - 2015/06/09/ PY - 2015/03/15/received PY - 2015/06/02/accepted PY - 2015/6/10/entrez PY - 2015/6/10/pubmed PY - 2016/10/8/medline KW - AMPK KW - Alzheimer’s disease KW - Amyloid-β KW - Mitochondrial biogenesis KW - PGC-1α KW - SIRT1 SP - 83 EP - 91 JF - Cellular and molecular neurobiology JO - Cell. Mol. Neurobiol. VL - 36 IS - 1 N2 - Mitochondrial biogenesis is involved in the regulation of mitochondrial content, morphology, and function. Impaired mitochondrial biogenesis has been observed in Alzheimer's disease. Amyloid-β (Aβ) has been shown to cause mitochondrial dysfunction in cultured neurons, but its role in mitochondrial biogenesis in neurons remains poorly defined. AMP-activated protein kinase (AMPK) and sirtuin 1 (SIRT1) are key energy-sensing molecules regulating mitochondrial biogenesis. In addition, peroxisome proliferator-activated receptor-γ coactivator 1-alpha (PGC-1α), the master regulator of mitochondrial biogenesis, is a target for SIRT1 deacetylase activity. In this study, we investigated the effects of Aβ25-35 on mitochondrial biogenesis in cultured hippocampal neurons and the underlying mechanisms. In primary hippocampal neurons, we found that 24-h incubation with Aβ25-35 suppressed both phosphorylations of AMPK and SIRT1 expression and increased PGC-1α acetylation expression. In addition, Aβ25-35 also resulted in a decrease in mitochondrial DNA copy number, as well as decreases in the expression of mitochondrial biogenesis factors (PGC-1α, NRF 1, NRF 2, and Tfam). Taken together, these data show that Aβ25-35 suppresses mitochondrial biogenesis in hippocampal neurons. Aβ25-35-induced impairment of mitochondrial biogenesis may be associated with the inhibition of the AMPK-SIRT1-PGC-1α pathway. SN - 1573-6830 UR - https://www.unboundmedicine.com/medline/citation/26055049/Aβ25_35_Suppresses_Mitochondrial_Biogenesis_in_Primary_Hippocampal_Neurons_ L2 - https://doi.org/10.1007/s10571-015-0222-6 DB - PRIME DP - Unbound Medicine ER -