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Study · In vitro (cells) · 2022

8 results

Kisspeptins inhibit human airway smooth muscle proliferation.

Borkar NA, Ambhore NS, Kalidhindi RSR, Pabelick CM, Prakash YS, Sathish V

JCI insight23 May 2022Cited by 16 (Europe PMC)

Summary

The text of this summary is not shown here, because the article license does not allow reuse. Read it at the source (opens in a new tab)

Text rights: Publisher copyright. Results still quote short attributed sentences.

Results from this study8

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

  1. 01LabIn vitro (cells)Efficacy outcome

    Cleaved forms of kisspeptin, particularly kisspeptin‑10, reduced PDGF-induced proliferation of human airway smooth muscle cells.

    In plain wordsIn cells, kisspeptin‑10 reduced the growth of human airway muscle cells stimulated by PDGF.

    Outcome
    DecreasePDGF-induced airway smooth muscle proliferation
    Study

    humann: not reported in source

    Human airway smooth muscle cells
    Outcome group
    Cell proliferation and differentiation · Respiratory
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Proliferation studies showed that cleaved forms of Kp, particularly Kp-10, mitigated PDGF-induced ASM proliferation.
  2. 02LabIn vitro (cells)Mechanism

    The antiproliferative effect of kisspeptin‑10 in airway smooth muscle cells was mediated by inhibition of the MAPK/ERK/Akt pathways.

    In plain wordsIn cells, kisspeptin‑10 slowed airway muscle cell growth by switching off the MAPK/ERK/Akt signalling pathways.

    Outcome
    DecreaseMAPK/ERK/Akt pathway activity
    Study

    humann: not reported in source

    Human airway smooth muscle cells
    Outcome group
    Receptor activity and mechanism · Respiratory
    Studied dose
    Dose not stated

    Source sentences

    Summary
    The antiproliferative effect of Kp-10 in ASM was mediated by inhibition of MAPK/ERK/Akt pathways
  3. 03LabIn vitro (cells)Mechanism

    Kisspeptin‑10 led to cell cycle arrest at the G0/G1 phase in airway smooth muscle cells.

    In plain wordsIn cells, kisspeptin‑10 stopped airway muscle cells at an early stage of the cell cycle.

    Outcome
    IncreaseCell cycle arrest at G0/G1
    Study

    humann: not reported in source

    Human airway smooth muscle cells
    Outcome group
    Receptor activity and mechanism · Respiratory
    Studied dose
    Dose not stated

    Source sentences

    Summary
    leading to cell cycle arrest at G0/G1 phase.
  4. 04LabIn vitro (cells)Mechanism

    Kisspeptin‑10 altered the expression of PCNA, C/EBP-α, Ki-67, cyclin D1 and cyclin E in airway smooth muscle cells. The direction is not stated.

    In plain wordsIn cells, kisspeptin‑10 changed the levels of several cell-growth proteins in airway muscle cells.

    Outcome
    Direction not reportedExpression of PCNA, C/EBP-α, Ki-67, cyclin D1 and cyclin E
    Study

    humann: not reported in source

    Human airway smooth muscle cells
    Outcome group
    Receptor activity and mechanism · Respiratory
    Studied dose
    Dose not stated

    Source sentences

    Summary
    with altered expression of PCNA, C/EBP-α, Ki-67, cyclin D1, and cyclin E

Natural levels measured3

These results measure the body's own peptide. Nobody was given the peptide. They are not evidence about taking it. They are left out of key results, evidence counts and charts.

  1. 05LabEndogenous levelEx vivo tissueOther

    Kisspeptin and KISS1R were expressed in human airways, especially in airway smooth muscle.

    In plain wordsIn human airway samples, the body's own kisspeptin and its receptor were present, especially in airway smooth muscle.

    Outcome
    Not applicableKisspeptin and KISS1R expression in human airways
    Study

    humann: not reported in source

    Outcome group
    Cell proliferation and differentiation · Respiratory

    Source sentences

    Summary
    We report potentially novel data indicating that Kp and KISS1R are expressed in human airways, especially ASM

    This result measures the body's own Kisspeptin-10. Nobody was given the peptide. It is not evidence about taking it.

  2. 06LabEndogenous levelEx vivo tissueOther

    Expression of kisspeptin and KISS1R was lower in airway smooth muscle from women than from men.

    In plain wordsIn human airway samples, the body's own kisspeptin and receptor levels were lower in samples from women than from men.

    Outcome
    DecreaseKisspeptin and KISS1R expression, women versus men
    Study

    humann: not reported in source

    Comparator
    Men
    Outcome group
    Cell proliferation and differentiation · Respiratory

    Source sentences

    Summary
    with lower expression in ASM from women compared with men and lower in patients with asthma compared with people without asthma.

    This result measures the body's own Kisspeptin-10. Nobody was given the peptide. It is not evidence about taking it.

  3. 07LabEndogenous levelEx vivo tissueOther

    Expression of kisspeptin and KISS1R in airway smooth muscle was lower in patients with asthma than in people without asthma.

    In plain wordsIn human airway samples, the body's own kisspeptin and receptor levels were lower in samples from patients with asthma than in samples without asthma.

    Outcome
    DecreaseKisspeptin and KISS1R expression, asthma versus no asthma
    Study

    humann: not reported in source

    Comparator
    People without asthma
    Outcome group
    Cell proliferation and differentiation · Respiratory

    Source sentences

    Summary
    lower in patients with asthma compared with people without asthma.

    This result measures the body's own Kisspeptin-10. Nobody was given the peptide. It is not evidence about taking it.

Studies that did not test the peptide alone1

In this study, Kisspeptin-10 was a lab tool or a carrier, part of a mix, or the subject of a lab method. These results are not evidence about taking Kisspeptin-10.

  1. 08LabNot a test of Kisspeptin-10 aloneIn vitro (cells)Mechanism

    Pharmacological inhibition and shRNA knockdown of the kisspeptin receptor KISS1R increased basal airway smooth muscle proliferation. This tests the receptor, not administered kisspeptin‑10.

    In plain wordsIn cells, blocking the kisspeptin receptor increased the growth of human airway muscle cells.

    Outcome
    IncreaseBasal ASM proliferation after KISS1R inhibition or knockdown
    Study

    humann: not reported in source

    Human airway smooth muscle cells
    Outcome group
    Cell proliferation and differentiation · Respiratory

    Source sentences

    Summary
    Pharmacological inhibition and shRNA knockdown of KISS1R increased basal ASM proliferation, which was further amplified by PDGF.

    In this study, Kisspeptin-10 was a lab tool or a carrier, part of a mix, or the subject of a lab method. This result is not evidence about taking Kisspeptin-10.

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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