Nicotinamide N-methyltransferase in endothelium protects against oxidant stress-induced endothelial injury.

Campagna R, Mateuszuk Ł, Wojnar-Lason K, Kaczara P, Tworzydło A, Kij A, Bujok R, Mlynarski J, Wang Y, Sartini D, Emanuelli M, Chlopicki S

Biochimica et biophysica acta. Molecular cell research19 Jun 2021Cited by 68 (Europe PMC)

PMID34153425DOI10.1016/j.bbamcr.2021.119082PepBankPUB-34153425

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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 study4

No result from this study comes from a test of the peptide.

Studies that did not test the peptide alone4

In this study, 5-amino-1MQ 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 5-amino-1MQ.

01LabNot a test of 5-amino-1MQ aloneIn vitro (cells)Mechanism
In endothelial cells, NNMT inhibition impaired MNA production.
In plain wordsIn cells, NNMT inhibition impaired MNA production.
Peptide
5-amino-1MQ
Outcome
DecreaseMNA production
Study
n: not reported in source
HAEC, HMEC-1 and EA.hy926 endothelial cells
Outcome group
Receptor activity and mechanism · Cardiovascular
Source sentences
Summary
Functional inhibition of NNMT was confirmed by LC/MS/MS-based analysis of impaired MNA production.
1 context sentence(design, population, supporting numbers)
Summary · context
NNMT in endothelial cells (HAEC, HMEC-1 and EA.hy926) was inhibited using two approaches: pharmacological inhibition of the enzyme by NNMT inhibitors (5-amino-1-methylquinoline - 5MQ and 6-methoxynicotinamide - JBSF-88) or by shRNA-mediated silencing.
In this study, 5-amino-1MQ 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 5-amino-1MQ.
Report a problemFND-3415342501
02LabNot a test of 5-amino-1MQ aloneIn vitro (cells)Mechanism
In endothelial cells exposed to menadione, NNMT inhibitors or gene silencing significantly decreased viability.
In plain wordsIn cells exposed to menadione, NNMT inhibitors or gene silencing significantly decreased endothelial viability.
Peptide
5-amino-1MQ
Outcome
DecreaseViability under menadione stress
Study
n: not reported in source
HAEC, HMEC-1 and EA.hy926 endothelial cells
Outcome group
Receptor activity and mechanism · Cardiovascular
Source sentences
Summary
The suppression of the NNMT activity either by NNMT inhibitors or shRNA-based silencing significantly decreased the endothelial cell viability in response to menadione.
1 context sentence(design, population, supporting numbers)
Summary · context
NNMT in endothelial cells (HAEC, HMEC-1 and EA.hy926) was inhibited using two approaches: pharmacological inhibition of the enzyme by NNMT inhibitors (5-amino-1-methylquinoline - 5MQ and 6-methoxynicotinamide - JBSF-88) or by shRNA-mediated silencing.
In this study, 5-amino-1MQ 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 5-amino-1MQ.
Report a problemFND-3415342502
03LabNot a test of 5-amino-1MQ aloneIn vitro (cells)Mechanism
In endothelial cells, NNMT inhibition decreased nuclear SIRT1 expression.
In plain wordsIn cells, NNMT inhibition decreased nuclear SIRT1 expression.
Peptide
5-amino-1MQ
Outcome
DecreaseNuclear SIRT1 expression
Study
n: not reported in source
HAEC, HMEC-1 and EA.hy926 endothelial cells
Outcome group
Receptor activity and mechanism · Cardiovascular
Source sentences
Summary
Furthermore, NNMT inhibition resulted in nuclear SIRT1 expression downregulation and upregulation of the phosphorylated form of SIRT1 on Ser47.
1 context sentence(design, population, supporting numbers)
Summary · context
NNMT in endothelial cells (HAEC, HMEC-1 and EA.hy926) was inhibited using two approaches: pharmacological inhibition of the enzyme by NNMT inhibitors (5-amino-1-methylquinoline - 5MQ and 6-methoxynicotinamide - JBSF-88) or by shRNA-mediated silencing.
In this study, 5-amino-1MQ 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 5-amino-1MQ.
Report a problemFND-3415342503
04LabNot a test of 5-amino-1MQ aloneIn vitro (cells)Mechanism
In endothelial cells, NNMT inhibition increased the Ser47-phosphorylated form of SIRT1.
In plain wordsIn cells, NNMT inhibition increased the Ser47-phosphorylated form of SIRT1.
Peptide
5-amino-1MQ
Outcome
IncreaseSIRT1 Ser47 phosphorylation
Study
n: not reported in source
HAEC, HMEC-1 and EA.hy926 endothelial cells
Outcome group
Receptor activity and mechanism · Cardiovascular
Source sentences
Summary
Furthermore, NNMT inhibition resulted in nuclear SIRT1 expression downregulation and upregulation of the phosphorylated form of SIRT1 on Ser47.
1 context sentence(design, population, supporting numbers)
Summary · context
NNMT in endothelial cells (HAEC, HMEC-1 and EA.hy926) was inhibited using two approaches: pharmacological inhibition of the enzyme by NNMT inhibitors (5-amino-1-methylquinoline - 5MQ and 6-methoxynicotinamide - JBSF-88) or by shRNA-mediated silencing.
In this study, 5-amino-1MQ 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 5-amino-1MQ.
Report a problemFND-3415342504

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
14 Oct 2026, 05:02 UTC
Study results updated
Version 1
14 Oct 2026, 01:46 UTC
First added · source update from Europe PMC

Subjects

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