Modulation of mitochondrial function by stem cell-derived cellular components

Liu, Tian, Im, Wooseok, Lee, Soon-Tae, Ban, Jae-Jun, Chai, Ye Jin, Lee, Mijung, Mook-Jung, Inhee, Chu, Kon and Kim, Manho (2014) Modulation of mitochondrial function by stem cell-derived cellular components. Biochemical and Biophysical Research Communications, 448 4: 403-408. doi:10.1016/j.bbrc.2014.04.129

Author Liu, Tian
Im, Wooseok
Lee, Soon-Tae
Ban, Jae-Jun
Chai, Ye Jin
Lee, Mijung
Mook-Jung, Inhee
Chu, Kon
Kim, Manho
Title Modulation of mitochondrial function by stem cell-derived cellular components
Journal name Biochemical and Biophysical Research Communications   Check publisher's open access policy
ISSN 1090-2104
Publication date 2014-06-13
Year available 2014
Sub-type Article (original research)
DOI 10.1016/j.bbrc.2014.04.129
Open Access Status
Volume 448
Issue 4
Start page 403
End page 408
Total pages 6
Place of publication Philadelphia, PA, United States
Publisher Elsevier
Collection year 2015
Language eng
Formatted abstract
Huntington’s disease (HD) is the most common hereditary neurodegenerative diseases, in which the loss of striatal neuron caused by the aggregation of mutant huntingtin protein (mHtt) is the main pathological feature. Our previous studies have demonstrated that human adipose stem cells (hASC) and its extracts can slow down the progression of HD in vitro and in vivo. hASC are readily accessible adult stem cells, and the cytosolic extracts contain a number of neurotrophic factors. Here, we further explored the role of the hASC extracts in neuronal death and mitochondrial function in HD. Our results showed that the hASC extracts prevent mHtt-induced cell toxicity and cell apoptosis. Moreover, the hASC extracts recovered mHtt-induced mitochondrial oxidative stress and reduced mitochondrial membrane potential. The hASC extracts blocked the interaction between p53 and mHtt, and decreased the endogenous p53 levels at both transcriptional and post-translational levels, resulting in the instability of p53 and increased neuronal survival. Taken together, these findings implicate protective roles of hASC extracts in mHtt-induced mitochondrial apoptosis, providing insights into the molecular mechanism of the hASC in the therapeutic strategy of HD.
Keyword Mutant huntingtin
Human adipose stem cells
Q-Index Code C1
Q-Index Status Confirmed Code
Institutional Status UQ

Document type: Journal Article
Sub-type: Article (original research)
Collections: Queensland Brain Institute Publications
Official 2015 Collection
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Citation counts: TR Web of Science Citation Count  Cited 4 times in Thomson Reuters Web of Science Article | Citations
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