The effects of a mitochondrial targeted peptide (elamipretide/SS31) on BAX recruitment and activation during apoptosis.

Grosser JA, Fehrman RL, Keefe D, Redmon M, Nickells RW

BMC research notes22 May 2021Cited by 7 (Europe PMC)

PMID34022923PMCIDPMC8141144DOI10.1186/s13104-021-05613-9PepBankPUB-34022923

Summary

ObjectiveElamipretide (SS31) is a mitochondria-targeted peptide that has reported functions of stabilizing mitochondrial cristae structure and improving mitochondrial bioenergetics. Several studies have documented cell protective features of this peptide, including impairment of intrinsic apoptosis by inhibiting the recruitment and activation of the pro-apoptotic BAX protein. We used live-cell imaging of ARPE-19 cells expressing fluorescently labeled BAX, cytochrome c, and a mitochondrial marker to investigate the effect of elamipretide on the kinetics of BAX recruitment, mitochondrial outer membrane permeabilization (as a function of cytochrome c release), and mitochondrial fragmentation, respectively.ResultIn nucleofected and plated ARPE-19 cells, elamipretide accelerated the formation of larger mitochondria. In the presence of the apoptotic stimulator, staurosporine, cells treated with elamipretide exhibited moderately slower rates of BAX recruitment. Peptide treatment, however, did not significantly delay the onset of BAX recruitment or the final total amount of BAX that was recruited. Additionally, elamipretide showed no impairment or delay of cytochrome c release or mitochondrial fragmentation, two events associated with normal BAX activation during cell death. These results indicate that the protective effect of elamipretide is not at the level of BAX activity to induce pro-apoptotic mitochondrial dysfunction after the initiation of staurosporine-induced apoptosis.

CC BYText from Europe PMC. Highlighted sentences are the source of results.

Results from this study6

6 results from studies that gave the peptide. No result from this study comes from people.

01LabIn vitro (cells)Mechanism
In ARPE-19 cells, elamipretide accelerated the formation of larger mitochondria.
In plain wordsIn lab retinal cells, elamipretide sped up the formation of larger mitochondria.
Peptide
Elamipretide (SS-31)
Outcome
IncreaseFormation of larger mitochondria
Study
n: not reported in source
Nucleofected and plated ARPE-19 cells
Outcome group
Mitochondrial function · Eye
Studied dose
Dose not stated
Source sentences
Summary
In nucleofected and plated ARPE-19 cells, elamipretide accelerated the formation of larger mitochondria.
1 context sentence(design, population, supporting numbers)
Summary · context
We used live-cell imaging of ARPE-19 cells expressing fluorescently labeled BAX, cytochrome c, and a mitochondrial marker to investigate the effect of elamipretide on the kinetics of BAX recruitment, mitochondrial outer membrane permeabilization (as a function of cytochrome c release), and mitochondrial fragmentation, respectively.
Show in the study text Report a problemFND-3402292301
02LabIn vitro (cells)Mechanism
In ARPE-19 cells exposed to staurosporine, elamipretide moderately slowed the rate of BAX recruitment.
In plain wordsIn lab retinal cells, elamipretide moderately slowed the arrival of the cell death protein BAX at mitochondria.
Peptide
Elamipretide (SS-31)
Outcome
DecreaseRate of BAX recruitment
Study
n: not reported in source
ARPE-19 cells with staurosporine-induced apoptosis
Outcome group
Cell viability and death · Eye
Studied dose
Dose not stated
Source sentences
Summary
In the presence of the apoptotic stimulator, staurosporine, cells treated with elamipretide exhibited moderately slower rates of BAX recruitment.
1 context sentence(design, population, supporting numbers)
Summary · context
We used live-cell imaging of ARPE-19 cells expressing fluorescently labeled BAX, cytochrome c, and a mitochondrial marker to investigate the effect of elamipretide on the kinetics of BAX recruitment, mitochondrial outer membrane permeabilization (as a function of cytochrome c release), and mitochondrial fragmentation, respectively.
Show in the study text Report a problemFND-3402292302
03LabIn vitro (cells)Mechanism
In ARPE-19 cells, elamipretide did not significantly delay the onset of BAX recruitment.
In plain wordsIn lab retinal cells, elamipretide did not significantly delay when the cell death protein BAX started to arrive.
Peptide
Elamipretide (SS-31)
Outcome
No significant changeOnset of BAX recruitment
Study
n: not reported in source
ARPE-19 cells with staurosporine-induced apoptosis
Outcome group
Cell viability and death · Eye
Studied dose
Dose not stated
Source sentences
Summary
Peptide treatment, however, did not significantly delay the onset of BAX recruitment or the final total amount of BAX that was recruited.
1 context sentence(design, population, supporting numbers)
Summary · context
We used live-cell imaging of ARPE-19 cells expressing fluorescently labeled BAX, cytochrome c, and a mitochondrial marker to investigate the effect of elamipretide on the kinetics of BAX recruitment, mitochondrial outer membrane permeabilization (as a function of cytochrome c release), and mitochondrial fragmentation, respectively.
Show in the study text Report a problemFND-3402292303
04LabIn vitro (cells)Mechanism
In ARPE-19 cells, elamipretide did not significantly change the final total amount of BAX recruited.
In plain wordsIn lab retinal cells, elamipretide did not significantly change the total amount of BAX that arrived.
Peptide
Elamipretide (SS-31)
Outcome
No significant changeTotal amount of BAX recruited
Study
n: not reported in source
ARPE-19 cells with staurosporine-induced apoptosis
Outcome group
Cell viability and death · Eye
Studied dose
Dose not stated
Source sentences
Summary
Peptide treatment, however, did not significantly delay the onset of BAX recruitment or the final total amount of BAX that was recruited.
1 context sentence(design, population, supporting numbers)
Summary · context
We used live-cell imaging of ARPE-19 cells expressing fluorescently labeled BAX, cytochrome c, and a mitochondrial marker to investigate the effect of elamipretide on the kinetics of BAX recruitment, mitochondrial outer membrane permeabilization (as a function of cytochrome c release), and mitochondrial fragmentation, respectively.
Show in the study text Report a problemFND-3402292304
05LabIn vitro (cells)Mechanism
In ARPE-19 cells, elamipretide did not impair or delay cytochrome c release.
In plain wordsIn lab retinal cells, elamipretide did not impair or delay the release of cytochrome c.
Peptide
Elamipretide (SS-31)
Outcome
No significant changeCytochrome c release
Study
n: not reported in source
ARPE-19 cells with staurosporine-induced apoptosis
Outcome group
Cell viability and death · Eye
Studied dose
Dose not stated
Source sentences
Summary
Additionally, elamipretide showed no impairment or delay of cytochrome c release or mitochondrial fragmentation, two events associated with normal BAX activation during cell death.
1 context sentence(design, population, supporting numbers)
Summary · context
We used live-cell imaging of ARPE-19 cells expressing fluorescently labeled BAX, cytochrome c, and a mitochondrial marker to investigate the effect of elamipretide on the kinetics of BAX recruitment, mitochondrial outer membrane permeabilization (as a function of cytochrome c release), and mitochondrial fragmentation, respectively.
Show in the study text Report a problemFND-3402292305
06LabIn vitro (cells)Mechanism
In ARPE-19 cells, elamipretide did not impair or delay mitochondrial fragmentation.
In plain wordsIn lab retinal cells, elamipretide did not impair or delay the splitting of mitochondria.
Peptide
Elamipretide (SS-31)
Outcome
No significant changeMitochondrial fragmentation
Study
n: not reported in source
ARPE-19 cells with staurosporine-induced apoptosis
Outcome group
Mitochondrial function · Eye
Studied dose
Dose not stated
Source sentences
Summary
Additionally, elamipretide showed no impairment or delay of cytochrome c release or mitochondrial fragmentation, two events associated with normal BAX activation during cell death.
1 context sentence(design, population, supporting numbers)
Summary · context
We used live-cell imaging of ARPE-19 cells expressing fluorescently labeled BAX, cytochrome c, and a mitochondrial marker to investigate the effect of elamipretide on the kinetics of BAX recruitment, mitochondrial outer membrane permeabilization (as a function of cytochrome c release), and mitochondrial fragmentation, respectively.
Show in the study text Report a problemFND-3402292306

AI wrote and checked these results. AI can make mistakes, so check important results against the source.

Version history

PepBank keeps every version of the data on this study. Status changes from Retraction Watch, Europe PMC and Crossref are listed with their source.

Version 2Current
10 Oct 2026, 08:19 UTC
Study results updated
Version 1
9 Oct 2026, 02:47 UTC
First added · source update from Europe PMC

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