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Study · In vitro (cells) · 2023

6 results

Kisspeptin-10 Mitigates α-Synuclein-Mediated Mitochondrial Apoptosis in SH-SY5Y-Derived Neurons via a Kisspeptin Receptor-Independent Manner.

Simon C, Soga T, Parhar I

International journal of molecular sciences23 Mar 2023Cited by 3 (Europe PMC)

PMID37047030 (opens in a new tab)PMCIDPMC10094180 (opens in a new tab)DOI10.3390/ijms24076056 (opens in a new tab)PepBankPUB-37047030
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Summary

The hypothalamic neurohormone kisspeptin-10 (KP-10) was inherently implicated in cholinergic pathologies when aberrant fluctuations of expression patterns and receptor densities were discerned in neurodegenerative micromilieus. That said, despite variable degrees of functional redundancy, KP-10, which is biologically governed by its cognate G-protein-coupled receptor, GPR54, attenuated the progressive demise of α-synuclein (α-syn)-rich cholinergic-like neurons. Under explicitly modeled environments, in silico algorithms further rationalized the surface complementarities between KP-10 and α-syn when KP-10 was unambiguously accommodated in the C-terminal binding pockets of α-syn. Indeed, the neuroprotective relevance of KP-10's binding mechanisms can be insinuated in the amelioration of α-syn-mediated neurotoxicity; yet it is obscure whether these extenuative circumstances are contingent upon prior GPR54 activation. Herein, choline acetyltransferase (ChAT)-positive SH-SY5Y neurons were engineered ad hoc to transiently overexpress human wild-type or E46K mutant α-syn while the mitigation of α-syn-induced neuronal death was ascertained via flow cytometric and immunocytochemical quantification. Recapitulating the specificity observed on cell viability, exogenously administered KP-10 (0.1 µM) substantially suppressed wild-type and E46K mutant α-syn-mediated apoptosis and mitochondrial depolarization in cholinergic differentiated neurons. In particular, co-administrations with a GPR54 antagonist, kisspeptin-234 (KP-234), failed to abrogate the robust neuroprotection elicited by KP-10, thereby signifying a GPR54 dispensable mechanism of action. Consistent with these observations, KP-10 treatment further diminished α-syn and ChAT immunoreactivity in neurons overexpressing wild-type and E46K mutant α-syn. Overall, these findings lend additional credence to the previous notion that KP-10's binding zone may harness efficacious moieties of neuroprotective intent.
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.

  1. 01LabIn vitro (cells)Efficacy outcome

    In SH-SY5Y-derived cholinergic neurons, KP-10 (0.1 µM) suppressed wild-type and E46K mutant α-synuclein-mediated apoptosis.

    In plain wordsIn human nerve-like cells grown in a dish, kisspeptin‑10 reduced cell death caused by the protein α-synuclein.

    Peptide
    Kisspeptin-10
    Outcome
    Decreaseα-Synuclein-mediated apoptosis
    Study

    humann: not reported in source

    ChAT-positive SH-SY5Y neurons overexpressing wild-type or E46K mutant α-synuclein
    Outcome group
    Neuroprotection · Nervous system and cognition
    Studied dose
    0.1 µM · in vitroAs given in this study (human).

    Source sentences

    Summary
    Recapitulating the specificity observed on cell viability, exogenously administered KP-10 (0.1 µM) substantially suppressed wild-type and E46K mutant α-syn-mediated apoptosis and mitochondrial depolarization in cholinergic differentiated neurons.
    1 context sentence
    Summary · context
    Herein, choline acetyltransferase (ChAT)-positive SH-SY5Y neurons were engineered ad hoc to transiently overexpress human wild-type or E46K mutant α-syn while the mitigation of α-syn-induced neuronal death was ascertained via flow cytometric and immunocytochemical quantification.
  2. 02LabIn vitro (cells)Efficacy outcome

    In SH-SY5Y-derived cholinergic neurons, KP-10 (0.1 µM) suppressed wild-type and E46K mutant α-synuclein-mediated mitochondrial depolarization.

    In plain wordsIn human nerve-like cells grown in a dish, kisspeptin‑10 reduced energy-unit damage caused by the protein α-synuclein.

    Peptide
    Kisspeptin-10
    Outcome
    Decreaseα-Synuclein-mediated mitochondrial depolarization
    Study

    humann: not reported in source

    ChAT-positive SH-SY5Y neurons overexpressing wild-type or E46K mutant α-synuclein
    Outcome group
    Neuroprotection · Nervous system and cognition
    Studied dose
    0.1 µM · in vitroAs given in this study (human).

    Source sentences

    Summary
    Recapitulating the specificity observed on cell viability, exogenously administered KP-10 (0.1 µM) substantially suppressed wild-type and E46K mutant α-syn-mediated apoptosis and mitochondrial depolarization in cholinergic differentiated neurons.
    1 context sentence
    Summary · context
    Herein, choline acetyltransferase (ChAT)-positive SH-SY5Y neurons were engineered ad hoc to transiently overexpress human wild-type or E46K mutant α-syn while the mitigation of α-syn-induced neuronal death was ascertained via flow cytometric and immunocytochemical quantification.
  3. 03LabIn vitro (cells)Mechanism

    In SH-SY5Y-derived neurons, adding the GPR54 antagonist KP-234 failed to abrogate the neuroprotection by KP-10.

    In plain wordsIn human nerve-like cells grown in a dish, blocking the kisspeptin receptor did not stop the protective effect of kisspeptin‑10.

    Peptide
    Kisspeptin-10
    Outcome
    Not applicableGPR54 dependence of KP-10 neuroprotection
    Study

    humann: not reported in source

    ChAT-positive SH-SY5Y neurons overexpressing wild-type or E46K mutant α-synuclein
    Outcome group
    Receptor activity and mechanism · Nervous system and cognition
    Studied dose
    0.1 µM · in vitroAs given in this study (human).

    Source sentences

    Summary
    In particular, co-administrations with a GPR54 antagonist, kisspeptin-234 (KP-234), failed to abrogate the robust neuroprotection elicited by KP-10, thereby signifying a GPR54 dispensable mechanism of action.
    1 context sentence
    Summary · context
    Herein, choline acetyltransferase (ChAT)-positive SH-SY5Y neurons were engineered ad hoc to transiently overexpress human wild-type or E46K mutant α-syn while the mitigation of α-syn-induced neuronal death was ascertained via flow cytometric and immunocytochemical quantification.
  4. 04LabIn vitro (cells)Mechanism

    In neurons overexpressing wild-type and E46K mutant α-synuclein, KP-10 treatment diminished α-synuclein immunoreactivity.

    In plain wordsIn human nerve-like cells grown in a dish, kisspeptin‑10 lowered the level of the protein α-synuclein.

    Peptide
    Kisspeptin-10
    Outcome
    Decreaseα-Synuclein immunoreactivity
    Study

    humann: not reported in source

    ChAT-positive SH-SY5Y neurons overexpressing wild-type or E46K mutant α-synuclein
    Outcome group
    Neuroprotection · Nervous system and cognition
    Studied dose
    0.1 µM · in vitroAs given in this study (human).

    Source sentences

    Summary
    Consistent with these observations, KP-10 treatment further diminished α-syn and ChAT immunoreactivity in neurons overexpressing wild-type and E46K mutant α-syn.
    1 context sentence
    Summary · context
    Herein, choline acetyltransferase (ChAT)-positive SH-SY5Y neurons were engineered ad hoc to transiently overexpress human wild-type or E46K mutant α-syn while the mitigation of α-syn-induced neuronal death was ascertained via flow cytometric and immunocytochemical quantification.
  5. 05LabIn vitro (cells)Mechanism

    In neurons overexpressing wild-type and E46K mutant α-synuclein, KP-10 treatment diminished ChAT immunoreactivity.

    In plain wordsIn human nerve-like cells grown in a dish, kisspeptin‑10 lowered the level of the enzyme ChAT.

    Peptide
    Kisspeptin-10
    Outcome
    DecreaseChAT immunoreactivity
    Study

    humann: not reported in source

    ChAT-positive SH-SY5Y neurons overexpressing wild-type or E46K mutant α-synuclein
    Outcome group
    Neuroprotection · Nervous system and cognition
    Studied dose
    0.1 µM · in vitroAs given in this study (human).

    Source sentences

    Summary
    Consistent with these observations, KP-10 treatment further diminished α-syn and ChAT immunoreactivity in neurons overexpressing wild-type and E46K mutant α-syn.
    1 context sentence
    Summary · context
    Herein, choline acetyltransferase (ChAT)-positive SH-SY5Y neurons were engineered ad hoc to transiently overexpress human wild-type or E46K mutant α-syn while the mitigation of α-syn-induced neuronal death was ascertained via flow cytometric and immunocytochemical quantification.
  6. 06Computer modelIn silicoMechanism

    In silico modelling placed KP-10 in the C-terminal binding pockets of α-synuclein.

    In plain wordsIn computer models, kisspeptin‑10 fitted into a binding pocket on the protein α-synuclein.

    Peptide
    Kisspeptin-10
    Outcome
    Not applicablePredicted binding of KP-10 to α-synuclein
    Study

    n: not reported in source

    in silico algorithms
    Outcome group
    Receptor activity and mechanism · Nervous system and cognition
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Under explicitly modeled environments, in silico algorithms further rationalized the surface complementarities between KP-10 and α-syn when KP-10 was unambiguously accommodated in the C-terminal binding pockets of α-syn.

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.

  1. Version 2Current

    10 Oct 2026, 09:43 UTC

    Study results updated

  2. Version 1

    9 Oct 2026, 03:04 UTC

    First added · source update from Europe PMC

Subjects

Terms as the source lists them.

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