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Crosstalk Between Histone and DNA Methylation in Regulation of Retinal Matrix Metalloproteinase-9 in Diabetes.

Abstract Diabetes activates matrix metalloproteinase-9 (MMP-9), and MMP-9 via damaging retinal mitochondria, activates capillary cell apoptosis. MMP-9 promoter has binding sites for many transcription factors, and in diabetes its promoter undergoes epigenetic modifications, including histone modifications and DNA methylation. Enhancer of Zeste homolog 2 (Ezh2), which catalyzes dimethylation/trimethylation of histone 3 lysine 27 (H3K27me2 and me3), is also associated with DNA methylation. Our aim was to investigate link(s) between histone and DNA modifications in the regulation of MMP-9.
PMID
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Authors

Mayor MeshTerms
Keywords
Journal Title investigative ophthalmology & visual science
Publication Year Start




PMID- 29261844
OWN - NLM
STAT- In-Process
LR  - 20171224
IS  - 1552-5783 (Electronic)
IS  - 0146-0404 (Linking)
VI  - 58
IP  - 14
DP  - 2017 Dec 1
TI  - Crosstalk Between Histone and DNA Methylation in Regulation of Retinal Matrix
      Metalloproteinase-9 in Diabetes.
PG  - 6440-6448
LID - 10.1167/iovs.17-22706 [doi]
AB  - Purpose: Diabetes activates matrix metalloproteinase-9 (MMP-9), and MMP-9 via
      damaging retinal mitochondria, activates capillary cell apoptosis. MMP-9 promoter
      has binding sites for many transcription factors, and in diabetes its promoter
      undergoes epigenetic modifications, including histone modifications and DNA
      methylation. Enhancer of Zeste homolog 2 (Ezh2), which catalyzes
      dimethylation/trimethylation of histone 3 lysine 27 (H3K27me2 and me3), is also
      associated with DNA methylation. Our aim was to investigate link(s) between
      histone and DNA modifications in the regulation of MMP-9. Methods: Using human
      retinal endothelial cells, and also retinal microvessels from diabetic rats,
      effect of hyperglycemia on H3K27me3, and recruitment of Ezh2 at the MMP-9
      promoter were quantified by chromatin-immunoprecipitation technique. Role of
      H3K27 trimethylation in regulating DNA methylation-transcription of MMP-9 was
      determined by regulating Ezh2 by its specific siRNA and also a pharmacologic
      inhibitor. Results: Hyperglycemia elevated H3K27me3 levels and the recruitment of
      Ezh2 at the MMP-9 promoter, and increased the enzyme activity of Ezh2. Inhibition
      of Ezh2 attenuated recruitment of both DNA methylating (Dnmt1) and
      hydroxymethylating (Tet2) enzymes and 5 hydroxymethyl cytosine at the same region
      of the MMP-9 promoter, and prevented increase in MMP-9 transcription and
      mitochondrial damage. Conclusions: Activation of Ezh2 in diabetes, via
      trimethylation of H3K27, facilitates recruitment of the enzymes responsible for
      regulation of DNA methylation of the MMP-9 promoter, resulting in its
      transcriptional activation. Thus, a close crosstalk between H3K27 trimethylation 
      and DNA methylation in diabetes plays a critical role in the maintenance of
      cellular epigenetic integrity of MMP-9.
FAU - Duraisamy, Arul J
AU  - Duraisamy AJ
AD  - Kresge Eye Institute, Wayne State University, Detroit, Michigan, United States.
FAU - Mishra, Manish
AU  - Mishra M
AD  - Kresge Eye Institute, Wayne State University, Detroit, Michigan, United States.
FAU - Kowluru, Renu A
AU  - Kowluru RA
AD  - Kresge Eye Institute, Wayne State University, Detroit, Michigan, United States.
LA  - eng
GR  - R01 EY014370/EY/NEI NIH HHS/United States
GR  - R01 EY017313/EY/NEI NIH HHS/United States
GR  - R01 EY022230/EY/NEI NIH HHS/United States
PT  - Journal Article
PL  - United States
TA  - Invest Ophthalmol Vis Sci
JT  - Investigative ophthalmology & visual science
JID - 7703701
PMC - PMC5737805
EDAT- 2017/12/21 06:00
MHDA- 2017/12/21 06:00
CRDT- 2017/12/21 06:00
PHST- 2017/12/21 06:00 [entrez]
PHST- 2017/12/21 06:00 [pubmed]
PHST- 2017/12/21 06:00 [medline]
AID - 2667223 [pii]
AID - 10.1167/iovs.17-22706 [doi]
PST - ppublish
SO  - Invest Ophthalmol Vis Sci. 2017 Dec 1;58(14):6440-6448. doi:
      10.1167/iovs.17-22706.