About: The interleukin-4/PPARγ signaling axis promotes oligodendrocyte differentiation and remyelination after brain injury

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About: The interleukin-4/PPARγ signaling axis promotes oligodendrocyte differentiation and remyelination after brain injury Goto Sponge NotDistinct Permalink

An Entity of Type : schema:ScholarlyArticle, within Data Space : wasabi.inria.fr associated with source document(s)

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	The interleukin-4/PPARγ signaling axis promotes oligodendrocyte differentiation and remyelination after brain injury
Creator	Chen, Jun Cai, Wei Dai, Xuejiao Gao, Yanqin Liu, Xiangrong Mu, Hongfeng Shi, Ligen Xu, Fei Zhang, Qingxiu Zhu, Wen Chenid, Jie Foleyid, Lesley Hitchensid, T Huid, Xiaoming Leakid, Rehana Shiid, Yejie
Source	PMC
abstract	The repair of white matter damage is of paramount importance for functional recovery after brain injuries. Here, we report that interleukin-4 (IL-4) promotes oligodendrocyte regeneration and remyelination. IL-4 receptor expression was detected in a variety of glial cells after ischemic brain injury, including oligodendrocyte lineage cells. IL-4 deficiency in knockout mice resulted in greater deterioration of white matter over 14 d after stroke. Consistent with these findings, intranasal delivery of IL-4 nanoparticles after stroke improved white matter integrity and attenuated long-term sensorimotor and cognitive deficits in wild-type mice, as revealed by histological immunostaining, electron microscopy, diffusion tensor imaging, and electrophysiology. The selective effect of IL-4 on remyelination was verified in an ex vivo organotypic model of demyelination. By leveraging primary oligodendrocyte progenitor cells (OPCs), microglia-depleted mice, and conditional OPC-specific peroxisome proliferator-activated receptor gamma (PPARγ) knockout mice, we discovered a direct salutary effect of IL-4 on oligodendrocyte differentiation that was mediated by the PPARγ axis. Our findings reveal a new regenerative role of IL-4 in the central nervous system (CNS), which lies beyond its known immunoregulatory functions on microglia/macrophages or peripheral lymphocytes. Therefore, intranasal IL-4 delivery may represent a novel therapeutic strategy to improve white matter integrity in stroke and other brain injuries.
has issue date	2019-06-21(xsd:dateTime)
bibo:doi	10.1371/journal.pbio.3000330
bibo:pmid	31226122
has license	cc-by
sha1sum (hex)	5719934f2cd95ffe4bd1aec0b7b9a314481aab60
schema:url	https://doi.org/10.1371/journal.pbio.3000330
resource representing a document's title	The interleukin-4/PPARγ signaling axis promotes oligodendrocyte differentiation and remyelination after brain injury
has PubMed Central identifier	PMC6608986
has PubMed identifier	31226122
schema:publication	PLoS Biol
resource representing a document's body	covid:5719934f2cd95ffe4bd1aec0b7b9a314481aab60#body_text
is schema:about of	named entity 'white matter' named entity 'cognitive deficits' named entity 'model' named entity 'knockout mice' named entity 'paramount' named entity 'revealed' named entity 'detected' named entity 'histological' named entity 'glial cells' named entity 'discovered' named entity 'AXIS' covid:arg/5719934f2cd95ffe4bd1aec0b7b9a314481aab60 named entity 'WHITE MATTER INTEGRITY' named entity 'REGENERATIVE' named entity 'HERE' named entity 'ROLE' named entity 'GLIAL CELLS' named entity 'REPRESENT' named entity 'SELECTIVE' named entity 'ISCHEMIC BRAIN INJURY' named entity 'STROKE' named entity 'LONG-TERM' named entity 'CONSISTENT WITH' named entity 'DELIVERY' named entity 'ATTENUATED' named entity 'MICE' named entity 'WILD-TYPE' named entity 'REPORT' named entity 'EX VIVO' named entity 'ORGANOTYPIC' named entity 'DETECTED' named entity 'VARIETY' named entity 'MEDIATED' named entity 'KNOCKOUT MICE' named entity 'LINEAGE' named entity 'DAMAGE' named entity 'DETERIORATION' named entity 'STRATEGY' named entity 'INTERLEUKIN-4 ' named entity 'NOVEL' named entity 'ITS' named entity 'OLIGODENDROCYTE' named entity 'HISTOLOGICAL' named entity 'REPAIR' named entity 'DEPLETED' named entity 'RECEPTOR' named entity 'LYMPHOCYTES' named entity 'OLIGODENDROCYTE DIFFERENTIATION' named entity 'BEYOND' named entity 'VERIFIED' named entity 'IL-4 RECEPTOR' named entity 'FUNCTIONAL RECOVERY' named entity 'OUR' named entity 'FUNCTIONS' named entity 'BRAIN INJURY' named entity 'AXIS' named entity 'DEFICIENCY' named entity 'NANOPARTICLES' named entity 'IMPROVED' named entity 'REVEALED' named entity 'PRIMARY' named entity 'CELLS' named entity 'SPECIFIC' named entity 'DIRECT' named entity 'KNOWN' named entity 'INCLUDING'

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