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Study · Animal study (in vivo) · mouse · 2017

22 results

Potent Vasoconstrictor Kisspeptin-10 Induces Atherosclerotic Plaque Progression and Instability: Reversal by its Receptor GPR54 Antagonist.

Sato K, Shirai R, Hontani M, Shinooka R, Hasegawa A, Kichise T, Yamashita T, Yoshizawa H, Watanabe R, Matsuyama TA, Ishibashi-Ueda H, Koba S, Kobayashi Y, Hirano T, Watanabe T

Journal of the American Heart Association14 Apr 2017Cited by 26 (Europe PMC)

PMID28411243 (opens in a new tab)PMCIDPMC5533042 (opens in a new tab)DOI10.1161/jaha.117.005790 (opens in a new tab)PepBankPUB-28411243
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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: CC BY-NC. Results still quote short attributed sentences.

Results from this study22

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

  1. 01AnimalAnimal study (in vivo)Efficacy outcome

    In ApoE-deficient mice, four-week infusion of KP-10 significantly accelerated development of aortic atherosclerotic lesions.

    In plain wordsIn mice prone to artery plaques, four weeks of KP-10 infusion sped up plaque development in the aorta.

    Peptide
    Kisspeptin-10
    Outcome
    IncreaseAortic atherosclerotic lesion development
    Study

    mousen: not reported in source

    ApoE-/- mice
    Outcome group
    Vascular function · Cardiovascular
    Studied dose
    Dose not stated · infusion · 4 weeksAs given in this study (mouse).

    Source sentences

    Summary
    Four-week-infusion of KP-10 into ApoE-/- mice significantly accelerated the development of aortic atherosclerotic lesions
    1 context sentence
    Summary · context
    We evaluated the effects of KP-10 on human umbilical vein endothelial cells, human monocyte-derived macrophages, human aortic smooth muscle cells in vitro, and atherosclerotic lesions in apolipoprotein E-deficient (ApoE-/-) mice in vivo.
  2. 02AnimalAnimal study (in vivo)Efficacy outcome

    In ApoE-deficient mice, four-week infusion of KP-10 increased monocyte/macrophage infiltration in lesions.

    In plain wordsIn mice prone to artery plaques, KP-10 infusion increased immune cell build-up in plaques.

    Peptide
    Kisspeptin-10
    Outcome
    IncreaseMonocyte/macrophage infiltration
    Study

    mousen: not reported in source

    ApoE-/- mice
    Outcome group
    Inflammation markers · Immune and inflammation
    Studied dose
    Dose not stated · infusion · 4 weeksAs given in this study (mouse).

    Source sentences

    Summary
    with increased monocyte/macrophage infiltration and vascular inflammation as well as decreased intraplaque vascular smooth muscle cells contents.
    1 context sentence
    Summary · context
    We evaluated the effects of KP-10 on human umbilical vein endothelial cells, human monocyte-derived macrophages, human aortic smooth muscle cells in vitro, and atherosclerotic lesions in apolipoprotein E-deficient (ApoE-/-) mice in vivo.
  3. 03AnimalAnimal study (in vivo)Efficacy outcome

    In ApoE-deficient mice, four-week infusion of KP-10 increased vascular inflammation.

    In plain wordsIn mice prone to artery plaques, KP-10 infusion increased inflammation in blood vessels.

    Peptide
    Kisspeptin-10
    Outcome
    IncreaseVascular inflammation
    Study

    mousen: not reported in source

    ApoE-/- mice
    Outcome group
    Inflammation markers · Immune and inflammation
    Studied dose
    Dose not stated · infusion · 4 weeksAs given in this study (mouse).

    Source sentences

    Summary
    with increased monocyte/macrophage infiltration and vascular inflammation as well as decreased intraplaque vascular smooth muscle cells contents.
    1 context sentence
    Summary · context
    We evaluated the effects of KP-10 on human umbilical vein endothelial cells, human monocyte-derived macrophages, human aortic smooth muscle cells in vitro, and atherosclerotic lesions in apolipoprotein E-deficient (ApoE-/-) mice in vivo.
  4. 04AnimalAnimal study (in vivo)Efficacy outcome

    In ApoE-deficient mice, four-week infusion of KP-10 decreased intraplaque vascular smooth muscle cell content.

    In plain wordsIn mice prone to artery plaques, KP-10 infusion reduced muscle cells inside plaques.

    Peptide
    Kisspeptin-10
    Outcome
    DecreaseIntraplaque vascular smooth muscle cell content
    Study

    mousen: not reported in source

    ApoE-/- mice
    Outcome group
    Vascular function · Cardiovascular
    Studied dose
    Dose not stated · infusion · 4 weeksAs given in this study (mouse).

    Source sentences

    Summary
    as well as decreased intraplaque vascular smooth muscle cells contents.
    1 context sentence
    Summary · context
    We evaluated the effects of KP-10 on human umbilical vein endothelial cells, human monocyte-derived macrophages, human aortic smooth muscle cells in vitro, and atherosclerotic lesions in apolipoprotein E-deficient (ApoE-/-) mice in vivo.
  5. 05LabIn vitro (cells)Mechanism

    In human umbilical vein endothelial cells, KP-10 significantly increased adhesion of human monocytes.

    In plain wordsIn human blood vessel cells in the lab, KP-10 increased monocyte sticking to the cells.

    Peptide
    Kisspeptin-10
    Outcome
    IncreaseMonocyte adhesion to HUVEC
    Study

    humann: not reported in source

    HUVEC and human monocytes
    Outcome group
    Vascular function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    KP-10 significantly increased the adhesion of human monocytes to human umbilical vein endothelial cells
    1 context sentence
    Summary · context
    We evaluated the effects of KP-10 on human umbilical vein endothelial cells, human monocyte-derived macrophages, human aortic smooth muscle cells in vitro, and atherosclerotic lesions in apolipoprotein E-deficient (ApoE-/-) mice in vivo.
  6. 06LabIn vitro (cells)Mechanism

    In human umbilical vein endothelial cells, KP-10 stimulated tumor necrosis factor-α mRNA expression.

    In plain wordsIn human blood vessel cells in the lab, KP-10 raised activity of the TNF-α gene.

    Peptide
    Kisspeptin-10
    Outcome
    IncreaseTNF-α mRNA in HUVEC
    Study

    humann: not reported in source

    HUVEC
    Outcome group
    Inflammation markers · Immune and inflammation
    Studied dose
    Dose not stated

    Source sentences

    Summary
    KP-10 stimulated mRNA expression of tumor necrosis factor-α, interleukin-6, monocyte chemotactic protein-1, intercellular adhesion molecule-1, vascular adhesion molecule-1, and E-selectin in human umbilical vein endothelial cells.
    1 context sentence
    Summary · context
    We evaluated the effects of KP-10 on human umbilical vein endothelial cells, human monocyte-derived macrophages, human aortic smooth muscle cells in vitro, and atherosclerotic lesions in apolipoprotein E-deficient (ApoE-/-) mice in vivo.
  7. 07LabIn vitro (cells)Mechanism

    In human umbilical vein endothelial cells, KP-10 stimulated interleukin-6 mRNA expression.

    In plain wordsIn human blood vessel cells in the lab, KP-10 raised activity of the IL-6 gene.

    Peptide
    Kisspeptin-10
    Outcome
    IncreaseIL-6 mRNA in HUVEC
    Study

    humann: not reported in source

    HUVEC
    Outcome group
    Inflammation markers · Immune and inflammation
    Studied dose
    Dose not stated

    Source sentences

    Summary
    KP-10 stimulated mRNA expression of tumor necrosis factor-α, interleukin-6, monocyte chemotactic protein-1, intercellular adhesion molecule-1, vascular adhesion molecule-1, and E-selectin in human umbilical vein endothelial cells.
    1 context sentence
    Summary · context
    We evaluated the effects of KP-10 on human umbilical vein endothelial cells, human monocyte-derived macrophages, human aortic smooth muscle cells in vitro, and atherosclerotic lesions in apolipoprotein E-deficient (ApoE-/-) mice in vivo.
  8. 08LabIn vitro (cells)Mechanism

    In human umbilical vein endothelial cells, KP-10 stimulated monocyte chemotactic protein-1 mRNA expression.

    In plain wordsIn human blood vessel cells in the lab, KP-10 raised activity of the MCP-1 gene.

    Peptide
    Kisspeptin-10
    Outcome
    IncreaseMCP-1 mRNA in HUVEC
    Study

    humann: not reported in source

    HUVEC
    Outcome group
    Inflammation markers · Immune and inflammation
    Studied dose
    Dose not stated

    Source sentences

    Summary
    KP-10 stimulated mRNA expression of tumor necrosis factor-α, interleukin-6, monocyte chemotactic protein-1, intercellular adhesion molecule-1, vascular adhesion molecule-1, and E-selectin in human umbilical vein endothelial cells.
    1 context sentence
    Summary · context
    We evaluated the effects of KP-10 on human umbilical vein endothelial cells, human monocyte-derived macrophages, human aortic smooth muscle cells in vitro, and atherosclerotic lesions in apolipoprotein E-deficient (ApoE-/-) mice in vivo.
  9. 09LabIn vitro (cells)Mechanism

    In human umbilical vein endothelial cells, KP-10 stimulated intercellular adhesion molecule-1 mRNA expression.

    In plain wordsIn human blood vessel cells in the lab, KP-10 raised activity of the ICAM-1 gene.

    Peptide
    Kisspeptin-10
    Outcome
    IncreaseICAM-1 mRNA in HUVEC
    Study

    humann: not reported in source

    HUVEC
    Outcome group
    Inflammation markers · Immune and inflammation
    Studied dose
    Dose not stated

    Source sentences

    Summary
    KP-10 stimulated mRNA expression of tumor necrosis factor-α, interleukin-6, monocyte chemotactic protein-1, intercellular adhesion molecule-1, vascular adhesion molecule-1, and E-selectin in human umbilical vein endothelial cells.
    1 context sentence
    Summary · context
    We evaluated the effects of KP-10 on human umbilical vein endothelial cells, human monocyte-derived macrophages, human aortic smooth muscle cells in vitro, and atherosclerotic lesions in apolipoprotein E-deficient (ApoE-/-) mice in vivo.
  10. 10LabIn vitro (cells)Mechanism

    In human umbilical vein endothelial cells, KP-10 stimulated vascular adhesion molecule-1 mRNA expression.

    In plain wordsIn human blood vessel cells in the lab, KP-10 raised activity of the VCAM-1 gene.

    Peptide
    Kisspeptin-10
    Outcome
    IncreaseVCAM-1 mRNA in HUVEC
    Study

    humann: not reported in source

    HUVEC
    Outcome group
    Inflammation markers · Immune and inflammation
    Studied dose
    Dose not stated

    Source sentences

    Summary
    KP-10 stimulated mRNA expression of tumor necrosis factor-α, interleukin-6, monocyte chemotactic protein-1, intercellular adhesion molecule-1, vascular adhesion molecule-1, and E-selectin in human umbilical vein endothelial cells.
    1 context sentence
    Summary · context
    We evaluated the effects of KP-10 on human umbilical vein endothelial cells, human monocyte-derived macrophages, human aortic smooth muscle cells in vitro, and atherosclerotic lesions in apolipoprotein E-deficient (ApoE-/-) mice in vivo.
  11. 11LabIn vitro (cells)Mechanism

    In human umbilical vein endothelial cells, KP-10 stimulated E-selectin mRNA expression.

    In plain wordsIn human blood vessel cells in the lab, KP-10 raised activity of the E-selectin gene.

    Peptide
    Kisspeptin-10
    Outcome
    IncreaseE-selectin mRNA in HUVEC
    Study

    humann: not reported in source

    HUVEC
    Outcome group
    Inflammation markers · Immune and inflammation
    Studied dose
    Dose not stated

    Source sentences

    Summary
    KP-10 stimulated mRNA expression of tumor necrosis factor-α, interleukin-6, monocyte chemotactic protein-1, intercellular adhesion molecule-1, vascular adhesion molecule-1, and E-selectin in human umbilical vein endothelial cells.
    1 context sentence
    Summary · context
    We evaluated the effects of KP-10 on human umbilical vein endothelial cells, human monocyte-derived macrophages, human aortic smooth muscle cells in vitro, and atherosclerotic lesions in apolipoprotein E-deficient (ApoE-/-) mice in vivo.
  12. 12LabIn vitro (cells)Mechanism

    In human monocyte-derived macrophages, KP-10 significantly enhanced oxidized low-density lipoprotein-induced foam cell formation.

    In plain wordsIn human immune cells in the lab, KP-10 increased foam cell formation caused by oxidized LDL.

    Peptide
    Kisspeptin-10
    Outcome
    IncreaseOxidized LDL-induced foam cell formation
    Study

    humann: not reported in source

    human monocyte-derived macrophages
    Outcome group
    Vascular function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    KP-10 significantly enhanced oxidized low-density lipoprotein-induced foam cell formation associated with upregulation of CD36 and acyl-CoA:cholesterol acyltransferase-1 in human monocyte-derived macrophages.
    1 context sentence
    Summary · context
    We evaluated the effects of KP-10 on human umbilical vein endothelial cells, human monocyte-derived macrophages, human aortic smooth muscle cells in vitro, and atherosclerotic lesions in apolipoprotein E-deficient (ApoE-/-) mice in vivo.
  13. 13LabIn vitro (cells)Mechanism

    In human monocyte-derived macrophages, KP-10 was associated with upregulation of CD36.

    In plain wordsIn human immune cells in the lab, KP-10 went with higher CD36 levels.

    Peptide
    Kisspeptin-10
    Outcome
    IncreaseCD36 upregulation in macrophages
    Study

    humann: not reported in source

    human monocyte-derived macrophages
    Outcome group
    Vascular function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    associated with upregulation of CD36 and acyl-CoA:cholesterol acyltransferase-1 in human monocyte-derived macrophages.
    1 context sentence
    Summary · context
    We evaluated the effects of KP-10 on human umbilical vein endothelial cells, human monocyte-derived macrophages, human aortic smooth muscle cells in vitro, and atherosclerotic lesions in apolipoprotein E-deficient (ApoE-/-) mice in vivo.
  14. 14LabIn vitro (cells)Mechanism

    In human monocyte-derived macrophages, KP-10 was associated with upregulation of acyl-CoA:cholesterol acyltransferase-1.

    In plain wordsIn human immune cells in the lab, KP-10 went with higher ACAT-1 levels.

    Peptide
    Kisspeptin-10
    Outcome
    IncreaseACAT-1 upregulation in macrophages
    Study

    humann: not reported in source

    human monocyte-derived macrophages
    Outcome group
    Vascular function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    associated with upregulation of CD36 and acyl-CoA:cholesterol acyltransferase-1 in human monocyte-derived macrophages.
    1 context sentence
    Summary · context
    We evaluated the effects of KP-10 on human umbilical vein endothelial cells, human monocyte-derived macrophages, human aortic smooth muscle cells in vitro, and atherosclerotic lesions in apolipoprotein E-deficient (ApoE-/-) mice in vivo.
  15. 15LabIn vitro (cells)Mechanism

    In human aortic smooth muscle cells, KP-10 significantly suppressed angiotensin II-induced migration.

    In plain wordsIn human artery muscle cells in the lab, KP-10 reduced angiotensin II-driven cell movement.

    Peptide
    Kisspeptin-10
    Outcome
    DecreaseAngiotensin II-induced migration
    Study

    humann: not reported in source

    human aortic smooth muscle cells
    Outcome group
    Vascular function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In human aortic smooth muscle cells, KP-10 significantly suppressed angiotensin II-induced migration and proliferation
    1 context sentence
    Summary · context
    We evaluated the effects of KP-10 on human umbilical vein endothelial cells, human monocyte-derived macrophages, human aortic smooth muscle cells in vitro, and atherosclerotic lesions in apolipoprotein E-deficient (ApoE-/-) mice in vivo.
  16. 16LabIn vitro (cells)Mechanism

    In human aortic smooth muscle cells, KP-10 significantly suppressed angiotensin II-induced proliferation.

    In plain wordsIn human artery muscle cells in the lab, KP-10 reduced angiotensin II-driven cell growth.

    Peptide
    Kisspeptin-10
    Outcome
    DecreaseAngiotensin II-induced proliferation
    Study

    humann: not reported in source

    human aortic smooth muscle cells
    Outcome group
    Vascular function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    In human aortic smooth muscle cells, KP-10 significantly suppressed angiotensin II-induced migration and proliferation
    1 context sentence
    Summary · context
    We evaluated the effects of KP-10 on human umbilical vein endothelial cells, human monocyte-derived macrophages, human aortic smooth muscle cells in vitro, and atherosclerotic lesions in apolipoprotein E-deficient (ApoE-/-) mice in vivo.
  17. 17LabIn vitro (cells)Mechanism

    In human aortic smooth muscle cells, KP-10 enhanced apoptosis.

    In plain wordsIn human artery muscle cells in the lab, KP-10 increased cell death.

    Peptide
    Kisspeptin-10
    Outcome
    IncreaseApoptosis in smooth muscle cells
    Study

    humann: not reported in source

    human aortic smooth muscle cells
    Outcome group
    Vascular function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    but enhanced apoptosis and activities of matrix metalloproteinase (MMP)-2 and MMP-9
    1 context sentence
    Summary · context
    We evaluated the effects of KP-10 on human umbilical vein endothelial cells, human monocyte-derived macrophages, human aortic smooth muscle cells in vitro, and atherosclerotic lesions in apolipoprotein E-deficient (ApoE-/-) mice in vivo.
  18. 18LabIn vitro (cells)Mechanism

    In human aortic smooth muscle cells, KP-10 enhanced the activities of matrix metalloproteinase-2 and matrix metalloproteinase-9.

    In plain wordsIn human artery muscle cells in the lab, KP-10 raised the activity of two tissue-degrading enzymes.

    Peptide
    Kisspeptin-10
    Outcome
    IncreaseMMP-2 and MMP-9 activities
    Study

    humann: not reported in source

    human aortic smooth muscle cells
    Outcome group
    Vascular function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    but enhanced apoptosis and activities of matrix metalloproteinase (MMP)-2 and MMP-9
    1 context sentence
    Summary · context
    We evaluated the effects of KP-10 on human umbilical vein endothelial cells, human monocyte-derived macrophages, human aortic smooth muscle cells in vitro, and atherosclerotic lesions in apolipoprotein E-deficient (ApoE-/-) mice in vivo.
  19. 19LabIn vitro (cells)Mechanism

    In human aortic smooth muscle cells, KP-10 was associated with upregulation of extracellular signal-regulated kinase 1 and 2 and p38.

    In plain wordsIn human artery muscle cells in the lab, KP-10 went with higher levels of two signaling proteins, ERK1/2 and p38.

    Peptide
    Kisspeptin-10
    Outcome
    IncreaseERK1/2 and p38 upregulation
    Study

    humann: not reported in source

    human aortic smooth muscle cells
    Outcome group
    Vascular function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    by upregulation of extracellular signal-regulated kinase 1 and 2, p38
    1 context sentence
    Summary · context
    We evaluated the effects of KP-10 on human umbilical vein endothelial cells, human monocyte-derived macrophages, human aortic smooth muscle cells in vitro, and atherosclerotic lesions in apolipoprotein E-deficient (ApoE-/-) mice in vivo.
  20. 20LabIn vitro (cells)Mechanism

    In human aortic smooth muscle cells, KP-10 was associated with upregulation of Bcl-2-associated X protein and caspase-3.

    In plain wordsIn human artery muscle cells in the lab, KP-10 went with higher levels of two cell-death proteins.

    Peptide
    Kisspeptin-10
    Outcome
    IncreaseBax and caspase-3 upregulation
    Study

    humann: not reported in source

    human aortic smooth muscle cells
    Outcome group
    Vascular function · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Bcl-2-associated X protein, and caspase-3.
    1 context sentence
    Summary · context
    We evaluated the effects of KP-10 on human umbilical vein endothelial cells, human monocyte-derived macrophages, human aortic smooth muscle cells in vitro, and atherosclerotic lesions in apolipoprotein E-deficient (ApoE-/-) mice in vivo.

Studies that did not test the peptide alone2

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. 21AnimalNot a test of Kisspeptin-10 aloneAnimal study (in vivo)Efficacy outcome

    In ApoE-deficient mice, infusion of the GPR54 antagonist P234 completely canceled the proatherosclerotic effects of endogenous and exogenous KP-10.

    In plain wordsIn mice prone to artery plaques, a GPR54 blocker fully cancelled the plaque-promoting effects of KP-10.

    Peptide
    Kisspeptin-10
    Outcome
    DecreaseKP-10 proatherosclerotic effects with P234
    Study

    mousen: not reported in source

    ApoE-/- mice
    Outcome group
    Vascular function · Cardiovascular

    Source sentences

    Summary
    Proatherosclerotic effects of endogenous and exogenous KP-10 were completely canceled by P234 infusion in ApoE-/- mice.
    1 context sentence
    Summary · context
    We evaluated the effects of KP-10 on human umbilical vein endothelial cells, human monocyte-derived macrophages, human aortic smooth muscle cells in vitro, and atherosclerotic lesions in apolipoprotein E-deficient (ApoE-/-) mice in vivo.

    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.

  2. 22LabNot a test of Kisspeptin-10 aloneIn vitro (cells)Mechanism

    In human umbilical vein endothelial cells, the GPR54 antagonist P234 significantly inhibited the KP-10-induced monocyte adhesion.

    In plain wordsIn human blood vessel cells in the lab, a GPR54 blocker stopped KP-10 from increasing monocyte sticking.

    Peptide
    Kisspeptin-10
    Outcome
    DecreaseKP-10-induced monocyte adhesion with P234
    Study

    humann: not reported in source

    HUVEC and human monocytes
    Outcome group
    Vascular function · Cardiovascular

    Source sentences

    Summary
    KP-10 significantly increased the adhesion of human monocytes to human umbilical vein endothelial cells, which was significantly inhibited by pretreatment with P234, a GPR54 antagonist.
    1 context sentence
    Summary · context
    We evaluated the effects of KP-10 on human umbilical vein endothelial cells, human monocyte-derived macrophages, human aortic smooth muscle cells in vitro, and atherosclerotic lesions in apolipoprotein E-deficient (ApoE-/-) mice in vivo.

    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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