Determining the Molecular Background of Endometrial Receptivity in Adenomyosis.
Adenomyosis
/ genetics
Adult
Case-Control Studies
Endometriosis
/ genetics
Endometrium
/ metabolism
Female
Gene Expression Profiling
Gene Expression Regulation
Gene Regulatory Networks
Humans
Infertility, Female
/ genetics
Interleukin-10
/ genetics
Interleukin-13
/ genetics
Interleukin-4
/ genetics
Interleukin-6
/ genetics
Leukemia Inhibitory Factor
/ genetics
Protein Interaction Mapping
Proto-Oncogene Proteins c-fos
/ genetics
Signal Transduction
Suppressor of Cytokine Signaling 3 Protein
/ genetics
Transcription Factors
/ genetics
adenomyosis
candidate genes
endometrial receptivity
endometriosis
gene expression
gene set enrichment analysis (GSEA)
multi-omics
protein–protein interaction network (PPIN)
Journal
Biomolecules
ISSN: 2218-273X
Titre abrégé: Biomolecules
Pays: Switzerland
ID NLM: 101596414
Informations de publication
Date de publication:
11 09 2020
11 09 2020
Historique:
received:
05
08
2020
revised:
02
09
2020
accepted:
09
09
2020
entrez:
16
9
2020
pubmed:
17
9
2020
medline:
25
6
2021
Statut:
epublish
Résumé
Adenomyosis is a gynaecological condition with limited evidence of negative impact to endometrial receptivity. It is commonly associated with endometriosis, which has been shown to alter endometrial expression patterns. Therefore, the candidate genes identified in endometriosis could serve as a source to study endometrial function in adenomyosis. Transcripts/proteins associated with endometrial receptivity in women with adenomyosis or endometriosis and healthy women were obtained from publications and their nomenclature was adopted according to the HUGO Gene Nomenclature Committee (HGNC). Retrieved genes were analysed for enriched pathways using Cytoscape/Search Tool for the Retrieval of Interacting Genes/Proteins (STRING) and Reactome tools to prioritise candidates for endometrial receptivity. These were used for validation on women with ( Functional enrichment analysis of 173, 42 and 151 genes associated with endometriosis, adenomyosis and healthy women, respectively, revealed signalling by interleukins and interleukin-4 and interleukin-13 signalling pathways, from which annotated This is the first integrative study providing putative candidate genes and pathways characterising endometrial receptivity in women with adenomyosis in comparison to healthy women and women with endometriosis.
Sections du résumé
BACKGROUND
Adenomyosis is a gynaecological condition with limited evidence of negative impact to endometrial receptivity. It is commonly associated with endometriosis, which has been shown to alter endometrial expression patterns. Therefore, the candidate genes identified in endometriosis could serve as a source to study endometrial function in adenomyosis.
METHODS
Transcripts/proteins associated with endometrial receptivity in women with adenomyosis or endometriosis and healthy women were obtained from publications and their nomenclature was adopted according to the HUGO Gene Nomenclature Committee (HGNC). Retrieved genes were analysed for enriched pathways using Cytoscape/Search Tool for the Retrieval of Interacting Genes/Proteins (STRING) and Reactome tools to prioritise candidates for endometrial receptivity. These were used for validation on women with (
RESULTS
Functional enrichment analysis of 173, 42 and 151 genes associated with endometriosis, adenomyosis and healthy women, respectively, revealed signalling by interleukins and interleukin-4 and interleukin-13 signalling pathways, from which annotated
CONCLUSION
This is the first integrative study providing putative candidate genes and pathways characterising endometrial receptivity in women with adenomyosis in comparison to healthy women and women with endometriosis.
Identifiants
pubmed: 32933042
pii: biom10091311
doi: 10.3390/biom10091311
pmc: PMC7563201
pii:
doi:
Substances chimiques
FOS protein, human
0
IL10 protein, human
0
IL13 protein, human
0
IL4 protein, human
0
IL6 protein, human
0
Interleukin-13
0
Interleukin-6
0
JunB protein, human
0
LIF protein, human
0
Leukemia Inhibitory Factor
0
Proto-Oncogene Proteins c-fos
0
SOCS3 protein, human
0
Suppressor of Cytokine Signaling 3 Protein
0
Transcription Factors
0
Interleukin-10
130068-27-8
Interleukin-4
207137-56-2
Types de publication
Journal Article
Research Support, Non-U.S. Gov't
Langues
eng
Sous-ensembles de citation
IM
Subventions
Organisme : Javna Agencija za Raziskovalno Dejavnost RS
ID : P3-0327
Pays : International
Organisme : Javna Agencija za Raziskovalno Dejavnost RS
ID : P4-0220
Pays : International
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