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Tytuł pozycji:

Caspase inhibition rescues F1Fo ATP synthase dysfunction-mediated dendritic spine elimination.

Tytuł:
Caspase inhibition rescues F1Fo ATP synthase dysfunction-mediated dendritic spine elimination.
Autorzy:
Chen H; Department of Biological Sciences, The University of Texas at Dallas, 800 west Campbell Rd, Richardson, TX, 75080, USA.
Tian J; Department of Biological Sciences, The University of Texas at Dallas, 800 west Campbell Rd, Richardson, TX, 75080, USA.
Guo L; Department of Biological Sciences, The University of Texas at Dallas, 800 west Campbell Rd, Richardson, TX, 75080, USA.; Higuchi Biosciences Center, The University of Kansas, Lawrence, KS, 66045, USA.
Du H; Department of Biological Sciences, The University of Texas at Dallas, 800 west Campbell Rd, Richardson, TX, 75080, USA. .; Higuchi Biosciences Center, The University of Kansas, Lawrence, KS, 66045, USA. .; Department of Pharmacology & Toxicology, The University of Kansas, Lawrence, KS, 66045, USA. .
Źródło:
Scientific reports [Sci Rep] 2020 Oct 16; Vol. 10 (1), pp. 17589. Date of Electronic Publication: 2020 Oct 16.
Typ publikacji:
Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't
Język:
English
Imprint Name(s):
Original Publication: London : Nature Publishing Group, copyright 2011-
MeSH Terms:
Dendritic Spines/*metabolism
Mitochondria/*metabolism
Mitochondrial Proton-Translocating ATPases/*metabolism
Adenosine Triphosphate/metabolism ; Amino Acid Chloromethyl Ketones/pharmacology ; Animals ; Caspase 3/metabolism ; Caspase Inhibitors/pharmacology ; Cell Death ; Female ; Hippocampus/metabolism ; Male ; Membrane Potential, Mitochondrial ; Mice ; Mice, Inbred C57BL ; Mitochondrial Proton-Translocating ATPases/physiology ; Neurons/metabolism ; Oligomycins/metabolism ; Oligomycins/pharmacology ; Quinolines/pharmacology ; Reactive Oxygen Species/metabolism
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Grant Information:
R01 AG053588 United States AG NIA NIH HHS; R00 AG037716 United States AG NIA NIH HHS; R01 AG059753 United States AG NIA NIH HHS; AARG-16-442863 United States ALZ Alzheimer's Association; R00AG037716 United States NH NIH HHS
Substance Nomenclature:
0 (Amino Acid Chloromethyl Ketones)
0 (Caspase Inhibitors)
0 (Oligomycins)
0 (Quinolines)
0 (Reactive Oxygen Species)
0 (quinoline-val-asp(OMe)-CH2-OPH)
05HQS4AI99 (oligomycin A)
8L70Q75FXE (Adenosine Triphosphate)
EC 3.4.22.- (Caspase 3)
EC 3.6.1.- (F1F0-ATP synthase)
EC 3.6.3.- (Mitochondrial Proton-Translocating ATPases)
Entry Date(s):
Date Created: 20201017 Date Completed: 20210112 Latest Revision: 20220929
Update Code:
20240105
PubMed Central ID:
PMC7568535
DOI:
10.1038/s41598-020-74613-9
PMID:
33067541
Czasopismo naukowe
Dendritic spine injury underlies synaptic failure in many neurological disorders. Mounting evidence suggests a mitochondrial pathway of local nonapoptotic caspase signaling in mediating spine pruning. However, it remains unclear whether this caspase signaling plays a key role in spine loss when severe mitochondrial functional defects are present. The answer to this question is critical especially for some pathological states, in which mitochondrial deficits are prominent and difficult to fix. F1Fo ATP synthase is a pivotal mitochondrial enzyme and the dysfunction of this enzyme involves in diseases with spinopathy. Here, we inhibited F1Fo ATP synthase function in primary cultured hippocampal neurons by using non-lethal oligomycin A treatment. Oligomycin A induced mitochondrial defects including collapsed mitochondrial membrane potential, dissipated ATP production, and elevated reactive oxygen species (ROS) production. In addition, dendritic mitochondria underwent increased fragmentation and reduced positioning to dendritic spines along with increased caspase 3 cleavage in dendritic shaft and spines in response to oligomycin A. Concurring with these dendritic mitochondrial changes, oligomycin A-insulted neurons displayed spine loss and altered spine architecture. Such oligomycin A-mediated changes in dendritic spines were substantially prevented by the inhibition of caspase activation by using a pan-caspase inhibitor, quinolyl-valyl-O-methylaspartyl-[-2,6-difluorophenoxy]-methyl ketone (Q-VD-OPh). Of note, the administration of Q-VD-OPh showed no protective effect on oligomycin A-induced mitochondrial dysfunction. Our findings suggest a pivotal role of caspase 3 signaling in mediating spine injury and the modulation of caspase 3 activation may benefit neurons from spine loss in diseases, at least, in those with F1Fo ATP synthase defects.
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