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Publication : The p38α MAPK Deletion in Oligodendroglia does not Attenuate Myelination Defects in a Mouse Model of Periventricular Leukomalacia.

First Author  Chung SH Year  2018
Journal  Neuroscience Volume  386
Pages  175-181 PubMed ID  29966722
Mgi Jnum  J:265052 Mgi Id  MGI:6196809
Doi  10.1016/j.neuroscience.2018.06.037 Citation  Chung SH, et al. (2018) The p38alpha MAPK Deletion in Oligodendroglia does not Attenuate Myelination Defects in a Mouse Model of Periventricular Leukomalacia. Neuroscience 386:175-181
abstractText  Periventricular leukomalacia (PVL) is a severe type of white matter damage in premature infants and the most common cause of cerebral palsy. It is generally known to be caused by hypoxia and inflammation. Currently there is no effective treatment available, in part due to that the pathogenesis of the disease has not been well understood. The p38alpha mitogen-activated protein kinase (MAPK) is the serine/threonine kinase and several in vitro studies demonstrated that p38 MAPK is essential for oligodendroglial differentiation and myelination. Indeed, our nerve/glial antigen 2 (NG2)-specific oligodendroglial p38alpha MAPK conditional knockout (CKO) mice revealed its complex roles in myelination and remyelination. To identify the specific in vivo roles of oligodendroglial p38alpha MAPK in PVL, we generated a mouse PVL model by combination of LPS-mediated inflammation and hypoxia-ischemia in NG2-p38alpha MAPK CKO mice. Our results demonstrate that a selective deletion of p38alpha MAPK in oligodendrocyte did not attenuate myelination defects in the mouse model of PVL. Myelination phenotype revealed by MBP immunostaining was not significantly affected in the p38alpha MAPK CKO mice compared to the wildtype after PVL induction. The electron microscopic images demonstrated that the microstructure of myelin structures was not significantly different between the wild-type and p38alpha MAPK CKO mice. In addition, oligodendrocyte degeneration in the corpus callosum white matter area was unaffected in the p38alpha MAPK CKO during and after the PVL induction. These data indicate that p38alpha MAPK in oligodendrocyte has minimal effect on myelination and oligodendrocyte survival in the mouse PVL model.
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