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Study · In vitro (cells) · 2018

11 results

Humanin prevents high glucose-induced monocyte adhesion to endothelial cells by targeting KLF2.

Wang X, Wu Z, He Y, Zhang H, Tian L, Zheng C, Shang T, Zhu Q, Li D, He Y

Molecular immunology18 Jul 2018Cited by 42 (Europe PMC)

PMID30029058 (opens in a new tab)DOI10.1016/j.molimm.2018.07.008 (opens in a new tab)PepBankPUB-30029058
Publisher pagePubMedAsk about this study
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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: Publisher copyright. Results still quote short attributed sentences.

Results from this study11

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

  1. 01LabIn vitro (cells)Mechanism

    In human umbilical vein endothelial cells, humanin treatment increased KLF2 expression at the transcriptional level.

    In plain wordsIn cells, humanin treatment raised KLF2, a regulator of blood vessel cell function.

    Peptide
    Humanin
    Outcome
    IncreaseKLF2 expression
    Study

    humann: not reported in source

    HUVECs
    Outcome group
    Receptor activity and mechanism · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Firstly, we found that humanin treatment induced the expression of Krüppel-like factor 2 (KLF2), an essential transcriptional regulator of endothelial function, at the transcriptional level in human umbilical vein endothelial cells (HUVECs).
  2. 02LabIn vitro (cells)Mechanism

    In human umbilical vein endothelial cells, humanin treatment regulated the expression of the KLF2 target gene eNOS.

    In plain wordsIn cells, humanin treatment changed the activity of eNOS, a gene that KLF2 controls.

    Peptide
    Humanin
    Outcome
    Direction not reportedeNOS expression (KLF2 target gene)
    Study

    humann: not reported in source

    HUVECs
    Outcome group
    Receptor activity and mechanism · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Additionally, our results indicate that humanin treatment regulated the expression of KLF2 target genes such as endothelial nitric oxide synthase (eNOS) and endothelin-1 (ET-1).
    1 context sentence
    Summary · context
    Firstly, we found that humanin treatment induced the expression of Krüppel-like factor 2 (KLF2), an essential transcriptional regulator of endothelial function, at the transcriptional level in human umbilical vein endothelial cells (HUVECs).
  3. 03LabIn vitro (cells)Mechanism

    In human umbilical vein endothelial cells, humanin treatment regulated the expression of the KLF2 target gene ET-1.

    In plain wordsIn cells, humanin treatment changed the activity of ET-1, a gene that KLF2 controls.

    Peptide
    Humanin
    Outcome
    Direction not reportedET-1 expression (KLF2 target gene)
    Study

    humann: not reported in source

    HUVECs
    Outcome group
    Receptor activity and mechanism · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Additionally, our results indicate that humanin treatment regulated the expression of KLF2 target genes such as endothelial nitric oxide synthase (eNOS) and endothelin-1 (ET-1).
    1 context sentence
    Summary · context
    Firstly, we found that humanin treatment induced the expression of Krüppel-like factor 2 (KLF2), an essential transcriptional regulator of endothelial function, at the transcriptional level in human umbilical vein endothelial cells (HUVECs).
  4. 04LabIn vitro (cells)Mechanism

    In human umbilical vein endothelial cells, the effect of humanin on KLF2 expression was mediated by phosphorylation of ERK5.

    In plain wordsIn cells, humanin raised KLF2 through a signal step called ERK5 phosphorylation.

    Peptide
    Humanin
    Outcome
    Not applicableERK5 phosphorylation as mediator of KLF2 induction
    Study

    humann: not reported in source

    HUVECs
    Outcome group
    Receptor activity and mechanism · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Evidence demonstrated that the effects of humanin on KLF2 expression was mediated by the phosphorylation of extracellular signal regulated kinase 5 (ERK5).
    1 context sentence
    Summary · context
    Firstly, we found that humanin treatment induced the expression of Krüppel-like factor 2 (KLF2), an essential transcriptional regulator of endothelial function, at the transcriptional level in human umbilical vein endothelial cells (HUVECs).
  5. 05LabIn vitro (cells)Mechanism

    In human umbilical vein endothelial cells exposed to high glucose, humanin restored the reduced KLF2 expression.

    In plain wordsIn cells exposed to high glucose, humanin brought back the lowered KLF2 level.

    Peptide
    Humanin
    Outcome
    IncreaseKLF2 expression under high glucose
    Study

    humann: not reported in source

    HUVECs
    Outcome group
    Receptor activity and mechanism · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Furthermore, humanin restored high glucose-induced reduction of KLF2 expression.
    1 context sentence
    Summary · context
    Firstly, we found that humanin treatment induced the expression of Krüppel-like factor 2 (KLF2), an essential transcriptional regulator of endothelial function, at the transcriptional level in human umbilical vein endothelial cells (HUVECs).
  6. 06LabIn vitro (cells)Mechanism

    In human umbilical vein endothelial cells, humanin significantly reduced the expression of VCAM-1.

    In plain wordsIn cells, humanin lowered VCAM-1, a molecule that helps immune cells stick to vessel cells.

    Peptide
    Humanin
    Outcome
    DecreaseVCAM-1 expression
    Study

    humann: not reported in source

    HUVECs
    Outcome group
    Inflammation markers · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    We also showed that humanin significantly reduced the expression of vascular cell adhesion molecule 1 (VCAM-1) and E-selectin.
    1 context sentence
    Summary · context
    Firstly, we found that humanin treatment induced the expression of Krüppel-like factor 2 (KLF2), an essential transcriptional regulator of endothelial function, at the transcriptional level in human umbilical vein endothelial cells (HUVECs).
  7. 07LabIn vitro (cells)Mechanism

    In human umbilical vein endothelial cells, humanin significantly reduced the expression of E-selectin.

    In plain wordsIn cells, humanin lowered E-selectin, a molecule that helps immune cells stick to vessel cells.

    Peptide
    Humanin
    Outcome
    DecreaseE-selectin expression
    Study

    humann: not reported in source

    HUVECs
    Outcome group
    Inflammation markers · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    We also showed that humanin significantly reduced the expression of vascular cell adhesion molecule 1 (VCAM-1) and E-selectin.
    1 context sentence
    Summary · context
    Firstly, we found that humanin treatment induced the expression of Krüppel-like factor 2 (KLF2), an essential transcriptional regulator of endothelial function, at the transcriptional level in human umbilical vein endothelial cells (HUVECs).
  8. 08LabIn vitro (cells)Efficacy outcome

    In human umbilical vein endothelial cells, humanin treatment markedly prevented high glucose-induced attachment of THP-1 monocytes.

    In plain wordsIn cells exposed to high glucose, humanin treatment reduced the sticking of immune cells to vessel cells.

    Peptide
    Humanin
    Outcome
    DecreaseTHP-1 monocyte attachment to HUVECs under high glucose
    Study

    humann: not reported in source

    HUVECs
    Outcome group
    Immune response · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Notably, humanin treatment markedly prevented high glucose-induced attachment of the monocyte THP-1 cells to HUVECs.
    1 context sentence
    Summary · context
    Firstly, we found that humanin treatment induced the expression of Krüppel-like factor 2 (KLF2), an essential transcriptional regulator of endothelial function, at the transcriptional level in human umbilical vein endothelial cells (HUVECs).
  9. 09LabIn vitro (cells)Efficacy outcome

    In human umbilical vein endothelial cells exposed to high glucose, humanin treatment inhibited secretion of TNF-α.

    In plain wordsIn cells exposed to high glucose, humanin treatment reduced release of the inflammation signal TNF-α.

    Peptide
    Humanin
    Outcome
    DecreaseTNF-α secretion under high glucose
    Study

    humann: not reported in source

    HUVECs
    Outcome group
    Inflammation markers · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Lastly, we report that humanin treatment inhibited high glucose-induced secretion of tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β).
    1 context sentence
    Summary · context
    Firstly, we found that humanin treatment induced the expression of Krüppel-like factor 2 (KLF2), an essential transcriptional regulator of endothelial function, at the transcriptional level in human umbilical vein endothelial cells (HUVECs).
  10. 10LabIn vitro (cells)Efficacy outcome

    In human umbilical vein endothelial cells exposed to high glucose, humanin treatment inhibited secretion of IL-1β.

    In plain wordsIn cells exposed to high glucose, humanin treatment reduced release of the inflammation signal IL-1β.

    Peptide
    Humanin
    Outcome
    DecreaseIL-1β secretion under high glucose
    Study

    humann: not reported in source

    HUVECs
    Outcome group
    Inflammation markers · Cardiovascular
    Studied dose
    Dose not stated

    Source sentences

    Summary
    Lastly, we report that humanin treatment inhibited high glucose-induced secretion of tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β).
    1 context sentence
    Summary · context
    Firstly, we found that humanin treatment induced the expression of Krüppel-like factor 2 (KLF2), an essential transcriptional regulator of endothelial function, at the transcriptional level in human umbilical vein endothelial cells (HUVECs).

Studies that did not test the peptide alone1

In this study, Humanin 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 Humanin.

  1. 11LabNot a test of Humanin aloneIn vitro (cells)Mechanism

    In human umbilical vein endothelial cells, knockdown of KLF2 abolished the effects of humanin treatment.

    In plain wordsIn cells, switching off the KLF2 gene removed the effects of humanin.

    Peptide
    Humanin
    Outcome
    Not applicableEffect of KLF2 knockdown on humanin effects
    Study

    humann: not reported in source

    HUVECs
    Outcome group
    Receptor activity and mechanism · Cardiovascular

    Source sentences

    Summary
    However, knockdown of KLF2 abolished these effects.
    1 context sentence
    Summary · context
    Firstly, we found that humanin treatment induced the expression of Krüppel-like factor 2 (KLF2), an essential transcriptional regulator of endothelial function, at the transcriptional level in human umbilical vein endothelial cells (HUVECs).

    In this study, Humanin 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 Humanin.

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

    13 Oct 2026, 21:44 UTC

    Study results updated

  2. Version 1

    13 Oct 2026, 16:31 UTC

    First added · source update from Europe PMC

Subjects

Terms as the source lists them.

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