Imbalance between HDAC and HAT activities drives aberrant STAT1/MyD88 expression in macrophages from type 1 diabetic mice
Aims To investigate the hypothesis that alteration in histone acetylation/deacetylation triggers aberrant STAT1/MyD88 expression in macrophages from diabetics. Increased STAT1/MyD88 expression is correlated with sterile inflammation in type 1 diabetic (T1D) mice. Methods To induce diabetes, we injected low-doses of streptozotocin in C57BL/6 mice. Peritoneal or bone marrow-differentiated macrophages were cultured in 5mM (low) or 25mM (high glucose). ChIP analysis of macrophages from nondiabetic or diabetic mice was performed to determine acetylation of lysine 9 in histone H3 in MyD88 and STAT1 promoter regions. Macrophages from diabetic mice were treated with the histone acetyltransferase inhibitor anacardic acid (AA), followed by determination of mRNA expression by qPCR. Results Increased STAT1 and MyD88 expression in macrophages from diabetic but not naive mice cultured in low glucose persisted for up to 6days. Macrophages from diabetic mice exhibited increased activity of histone acetyltransferases (HAT) and decreased histone deacetylases (HDAC) activity. We detected increased H3K9Ac binding toStat1/Myd88promoters in macrophages from T1D mice and AAin vitrotreatment reduced STAT1 and MyD88 mRNA expression. Conclusions/interpretation These results indicate that histone acetylation drives elevated Stat1/Myd88 expression in macrophages from diabetic mice, and this mechanism may be involved in sterile inflammation and diabetes comorbidities..
| Medienart: |
Artikel |
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| Erscheinungsjahr: |
2017 |
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| Erschienen: |
2017 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:31 |
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| Enthalten in: |
Journal of diabetes and its complications - 31(2017), 2, Seite 334-339 |
| Sprache: |
Englisch |
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| Beteiligte Personen: |
Filgueiras, Luciano Ribeiro [VerfasserIn] |
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| Links: |
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| Themen: |
Animals |
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| doi: |
10.1016/j.jdiacomp.2016.08.001 |
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| funding: |
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OLC1991045336 |
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| 100 | 1 | |a Filgueiras, Luciano Ribeiro |e verfasserin |4 aut | |
| 245 | 1 | 0 | |a Imbalance between HDAC and HAT activities drives aberrant STAT1/MyD88 expression in macrophages from type 1 diabetic mice |
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| 520 | |a Aims To investigate the hypothesis that alteration in histone acetylation/deacetylation triggers aberrant STAT1/MyD88 expression in macrophages from diabetics. Increased STAT1/MyD88 expression is correlated with sterile inflammation in type 1 diabetic (T1D) mice. Methods To induce diabetes, we injected low-doses of streptozotocin in C57BL/6 mice. Peritoneal or bone marrow-differentiated macrophages were cultured in 5mM (low) or 25mM (high glucose). ChIP analysis of macrophages from nondiabetic or diabetic mice was performed to determine acetylation of lysine 9 in histone H3 in MyD88 and STAT1 promoter regions. Macrophages from diabetic mice were treated with the histone acetyltransferase inhibitor anacardic acid (AA), followed by determination of mRNA expression by qPCR. Results Increased STAT1 and MyD88 expression in macrophages from diabetic but not naive mice cultured in low glucose persisted for up to 6days. Macrophages from diabetic mice exhibited increased activity of histone acetyltransferases (HAT) and decreased histone deacetylases (HDAC) activity. We detected increased H3K9Ac binding toStat1/Myd88promoters in macrophages from T1D mice and AAin vitrotreatment reduced STAT1 and MyD88 mRNA expression. Conclusions/interpretation These results indicate that histone acetylation drives elevated Stat1/Myd88 expression in macrophages from diabetic mice, and this mechanism may be involved in sterile inflammation and diabetes comorbidities. | ||
| 650 | 4 | |a Gene expression | |
| 650 | 4 | |a Animals | |
| 650 | 4 | |a Hyperglycemia | |
| 650 | 4 | |a Chromatin | |
| 650 | 4 | |a Bone marrow | |
| 650 | 4 | |a Deoxyribonucleic acid--DNA | |
| 650 | 4 | |a Epigenetics | |
| 650 | 4 | |a Metabolism | |
| 650 | 4 | |a Immunoglobulins | |
| 650 | 4 | |a Diabetes | |
| 650 | 4 | |a Inflammation | |
| 700 | 1 | |a Brandt, Stephanie L |4 oth | |
| 700 | 1 | |a Ramalho, Theresa Raquel de Oliveira |4 oth | |
| 700 | 1 | |a Jancar, Sonia |4 oth | |
| 700 | 1 | |a Serezani, C. Henrique |4 oth | |
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| 773 | 1 | 8 | |g volume:31 |g year:2017 |g number:2 |g pages:334-339 |
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