DNA methylation of the human oxytocin receptor gene promoter regulates tissue-specific gene suppression.

Kusui C, Kimura T, Ogita K, Nakamura H, Matsumura Y, Koyama M, Azuma C, Murata Y

Biochemical and biophysical research communications1 Dec 2001Cited by 148 (Europe PMC)

PMID11726201DOI10.1006/bbrc.2001.6024PepBankPUB-11726201

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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, Oxytocin 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 Oxytocin.

01LabNot a test of Oxytocin aloneEx vivo tissueMechanism
The oxytocin receptor gene CpG island was most highly methylated in liver, where the gene is inactivated.
In plain wordsIn human tissue samples, the oxytocin receptor gene was most methylated in liver, where it is switched off.
Peptide
Oxytocin
Outcome
Not applicableMethylation of the OTR CpG island across tissues
Study
humann: not reported in source
Human leukocytes, myometrium and liver
Outcome group
Receptor activity and mechanism · Endocrine and hormones
Source sentences
Summary
The amount of PCR products was largest in the liver, suggesting that this CpG island in the OTR gene is most highly methylated in liver, where the gene is always inactivated.
1 context sentence(design, population, supporting numbers)
Summary · context
We estimated the level of methylation within the CpG islands of the OTR gene in peripheral blood leukocytes, nonpregnant uterine myometrium, term uterine myometrium and liver.
In this study, Oxytocin 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 Oxytocin.
Report a problemFND-1172620102
02LabNot a test of Oxytocin aloneIn vitro (cells)Mechanism
In HepG2 cells, the demethylating agent 5-azacytidine increased oxytocin receptor mRNA in a dose-dependent manner.
In plain wordsIn human liver-tumour cells, a drug that removes methylation raised oxytocin receptor messenger RNA.
Peptide
Oxytocin
Outcome
IncreaseOTR mRNA after demethylating agent
Study
humann: not reported in source
HepG2 cells
Comparator
Untreated cells
Outcome group
Receptor activity and mechanism · Endocrine and hormones
Source sentences
Summary
Semiquantitative RT-PCR indicated that OTR mRNA was significantly increased by Aza-C treatment in a dose-dependent manner.
1 context sentence(design, population, supporting numbers)
Summary · context
HepG2 derived from human hepatoblastoma, in which OTR gene transcription was suppressed, was treated with a demethylating agent, 5-azacytidine (Aza-C) for 2 days.
In this study, Oxytocin 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 Oxytocin.
Report a problemFND-1172620101
03LabNot a test of Oxytocin aloneIn vitro (cells)Mechanism
In HepG2 cells, methylation suppressed reporter activity of a construct with the CpG island to 30.6% of control, against 81.4% for a construct without it.
In plain wordsIn cells, methylation cut activity of a receptor gene construct to 30.6% of control, but only to 81.4% without the CpG island.
Peptide
Oxytocin
Outcome
DecreaseReporter activity after methylation, CpG island present
Study
humann: not reported in source
HepG2 cells, reporter plasmid
Comparator
Unmethylated control
Outcome group
Receptor activity and mechanism · Endocrine and hormones
Measurements
Reporter activity with CpG island
30.6 % of control
-2860/+1342-GL3
Reporter activity without CpG island
81.4 % of control
-2840/+144-GL3
Source sentences
Summary
The reporter gene activity of expression plasmid -2860/+1342-GL3, containing the CpG island, in HepG2 cells was suppressed to 30.6% of the control level after methylation with SssI methylase, while that of -2840/+144-GL3, without the CpG island was suppressed only to 81.4%.
In this study, Oxytocin 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 Oxytocin.
Report a problemFND-1172620103
04LabNot a test of Oxytocin aloneIn vitro (cells)Mechanism
In HepG2 cells, deleting the MT2 segment rescued reporter activity to a suppression rate of 68.0%.
In plain wordsIn cells, removing one methylation-sensitive segment of the receptor gene construct partly restored its activity.
Peptide
Oxytocin
Outcome
IncreaseRescue of reporter activity by MT2 deletion
Study
humann: not reported in source
HepG2 cells, reporter plasmid
Outcome group
Receptor activity and mechanism · Endocrine and hormones
Measurements
Suppression rate after MT2 deletion
68%
-2860/+1342(del)MT2-GL3
Source sentences
Summary
The deletion of the segment (MT2) where the level of methylation was most different between liver and uterus (-2860/+1342(del)MT2-GL3) rescued the suppression rate to 68.0%.
In this study, Oxytocin 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 Oxytocin.
Report a problemFND-1172620104

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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
11 Oct 2026, 20:03 UTC
Study results updated
Version 1
9 Oct 2026, 02:52 UTC
First added · source update from Europe PMC

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