Genetic and epigenetic-sensitive regulatory network in immune response : a putative link between HLA-G and diabetes
INTRODUCTION: Human leukocyte antigen-G (HLA-G) gene encodes for a tolerogenic molecule constitutively expressed in human pancreas and upregulated upon inflammatory signals. The 14 bp INS/DEL polymorphism in the 3'UTR of HLA-G may influence the susceptibility for diabetes and coronary heart diseases (CHD), thus suggesting a novel candidate gene. DNA hypomethylation at HLA-G promoter may be a putative useful clinical biomarker for CHD onset. Upregulation of soluble HLA-G isoform (sHLA-G) was detected in prediabetic and diabetic subjects, suggesting a putative role in metabolic dysfunctions.
AREAS COVERED: We conducted a scoping literature review of genetic and epigenetic-sensitive mechanisms regulating HLA-G in diabetes. English-language manuscripts published between 1997 and 2019, were identified through PubMed, Google Scholar, and Web of Science database searches. After selecting 14 original articles representing case-control studies, we summarized and critically evaluated their main findings.
EXPERT COMMENTARY: Although epigenetic modifications are involved in the onset of hyperglycemic conditions evolving into diabetes and CHD, it is still difficult to obtain simple and useful clinical biomarkers. Inflammatory-induced KDM6A/INF-β/HLA-G axis might be a part of the epigenetic network leading to overexpression of HLA-G at pancreatic level. Network medicine may show whether HLA-G is involved in diabetes and CHD.
| Medienart: |
E-Artikel |
|---|
| Erscheinungsjahr: |
2019 |
|---|---|
| Erschienen: |
2019 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:14 |
|---|---|
| Enthalten in: |
Expert review of endocrinology & metabolism - 14(2019), 4 vom: 04. Juli, Seite 233-241 |
| Sprache: |
Englisch |
|---|
| Beteiligte Personen: |
Sommese, Linda [VerfasserIn] |
|---|
| Links: |
|---|
| Themen: |
3' Untranslated Regions |
|---|
| Anmerkungen: |
Date Completed 06.07.2020 Date Revised 06.07.2020 published: Print-Electronic Citation Status MEDLINE |
|---|
| doi: |
10.1080/17446651.2019.1620103 |
|---|
| funding: |
|
|---|---|
| Förderinstitution / Projekttitel: |
|
| PPN (Katalog-ID): |
NLM29749774X |
|---|
| LEADER | 01000naa a22002652 4500 | ||
|---|---|---|---|
| 001 | NLM29749774X | ||
| 003 | DE-627 | ||
| 005 | 20231225092124.0 | ||
| 007 | cr uuu---uuuuu | ||
| 008 | 231225s2019 xx |||||o 00| ||eng c | ||
| 024 | 7 | |a 10.1080/17446651.2019.1620103 |2 doi | |
| 028 | 5 | 2 | |a pubmed24n0991.xml |
| 035 | |a (DE-627)NLM29749774X | ||
| 035 | |a (NLM)31131681 | ||
| 040 | |a DE-627 |b ger |c DE-627 |e rakwb | ||
| 041 | |a eng | ||
| 100 | 1 | |a Sommese, Linda |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a Genetic and epigenetic-sensitive regulatory network in immune response |b a putative link between HLA-G and diabetes |
| 264 | 1 | |c 2019 | |
| 336 | |a Text |b txt |2 rdacontent | ||
| 337 | |a ƒaComputermedien |b c |2 rdamedia | ||
| 338 | |a ƒa Online-Ressource |b cr |2 rdacarrier | ||
| 500 | |a Date Completed 06.07.2020 | ||
| 500 | |a Date Revised 06.07.2020 | ||
| 500 | |a published: Print-Electronic | ||
| 500 | |a Citation Status MEDLINE | ||
| 520 | |a INTRODUCTION: Human leukocyte antigen-G (HLA-G) gene encodes for a tolerogenic molecule constitutively expressed in human pancreas and upregulated upon inflammatory signals. The 14 bp INS/DEL polymorphism in the 3'UTR of HLA-G may influence the susceptibility for diabetes and coronary heart diseases (CHD), thus suggesting a novel candidate gene. DNA hypomethylation at HLA-G promoter may be a putative useful clinical biomarker for CHD onset. Upregulation of soluble HLA-G isoform (sHLA-G) was detected in prediabetic and diabetic subjects, suggesting a putative role in metabolic dysfunctions | ||
| 520 | |a AREAS COVERED: We conducted a scoping literature review of genetic and epigenetic-sensitive mechanisms regulating HLA-G in diabetes. English-language manuscripts published between 1997 and 2019, were identified through PubMed, Google Scholar, and Web of Science database searches. After selecting 14 original articles representing case-control studies, we summarized and critically evaluated their main findings | ||
| 520 | |a EXPERT COMMENTARY: Although epigenetic modifications are involved in the onset of hyperglycemic conditions evolving into diabetes and CHD, it is still difficult to obtain simple and useful clinical biomarkers. Inflammatory-induced KDM6A/INF-β/HLA-G axis might be a part of the epigenetic network leading to overexpression of HLA-G at pancreatic level. Network medicine may show whether HLA-G is involved in diabetes and CHD | ||
| 650 | 4 | |a Journal Article | |
| 650 | 4 | |a Research Support, Non-U.S. Gov't | |
| 650 | 4 | |a Review | |
| 650 | 4 | |a HLA-G | |
| 650 | 4 | |a diabetes | |
| 650 | 4 | |a epigenetics | |
| 650 | 4 | |a inflammation | |
| 650 | 4 | |a network medicine | |
| 650 | 4 | |a polymorphism | |
| 650 | 7 | |a 3' Untranslated Regions |2 NLM | |
| 650 | 7 | |a HLA-G Antigens |2 NLM | |
| 700 | 1 | |a Benincasa, Giuditta |e verfasserin |4 aut | |
| 700 | 1 | |a Schiano, Concetta |e verfasserin |4 aut | |
| 700 | 1 | |a Marfella, Raffaele |e verfasserin |4 aut | |
| 700 | 1 | |a Grimaldi, Vincenzo |e verfasserin |4 aut | |
| 700 | 1 | |a Sorriento, Antonio |e verfasserin |4 aut | |
| 700 | 1 | |a Lucchese, Roberta |e verfasserin |4 aut | |
| 700 | 1 | |a Fiorito, Carmela |e verfasserin |4 aut | |
| 700 | 1 | |a Sardu, Celestino |e verfasserin |4 aut | |
| 700 | 1 | |a Nicoletti, Giovanni Francesco |e verfasserin |4 aut | |
| 700 | 1 | |a Napoli, Claudio |e verfasserin |4 aut | |
| 773 | 0 | 8 | |i Enthalten in |t Expert review of endocrinology & metabolism |d 2006 |g 14(2019), 4 vom: 04. Juli, Seite 233-241 |w (DE-627)NLM191111503 |x 1744-8417 |7 nnns |
| 773 | 1 | 8 | |g volume:14 |g year:2019 |g number:4 |g day:04 |g month:07 |g pages:233-241 |
| 856 | 4 | 0 | |u http://dx.doi.org/10.1080/17446651.2019.1620103 |3 Volltext |
| 912 | |a GBV_USEFLAG_A | ||
| 912 | |a GBV_NLM | ||
| 951 | |a AR | ||
| 952 | |d 14 |j 2019 |e 4 |b 04 |c 07 |h 233-241 | ||