Premium
Epigenetic Modifications Following NLRP3 Induced Inflammation of Oligodendrocyte Precursor Cells
Author(s) -
McKinley Raechel Elaine,
Csoka Antonei
Publication year - 2017
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.31.1_supplement.lb38
Subject(s) - epigenetics , oligodendrocyte , inflammation , neuroscience , dna methylation , myelin , biology , multiple sclerosis , progenitor cell , microbiology and biotechnology , embryonic stem cell , microglia , central nervous system , immunology , stem cell , genetics , gene expression , gene
Mature Oligodendrocytes (OCs) are specialized cells in the central nervous system that have the ability wrap their cytoplasm around the axons of neurons to makemyelin. Myelin is the lipid‐rich covering of axons that is responsible for fast salutatory conduction in synaptic transmission. As opposed to many cell types in the central nervous system, OCs have pools of readily available progenitor cells called Oligodendrocyte Precursor Cells (OPCs), that during normal repair will replace the damaged mature OCs. However, when damage is done to OCs in disorders such as multiple sclerosis, stroke, and spinal cord injury, this phenomenon does not take place. In previous studies, it has been shown that epigenetics is vital to the maturation of OPCs during embryonic development and differentiation. In this study, we analyzed the epigenetic modifications including DNA methylation in NLRP3‐induced inflammation of OPCs. Using microarray technology, we analyzed the genome‐wide DNA from OPC cells to find the global epigenetic modifications that take place during NLRP3‐activated inflammation. Support or Funding Information National Institute of Health (NIH) R25 Resource Grant. (1 R25 AG047843‐01)