Proteomics

Dataset Information

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Oxygen effect on murine progenitor oligodrendrocytes


ABSTRACT: Hyperoxia is known to cause cerebral white matter injury in preterm infants with male sex being identified as an independent risk factor for poor neurodevelopmental outcome. We investigated the underlying mechanisms behind such a sex dependent difference by a comaparative protein profiling of male and female murine progenitor oligodendrocytes treated with 3 % or 80% oxygen. We demonstrate that following hyperoxia, the male derived oligodendrocyte progenitor cells (OPCs) are severely affected with respect to their energy metabolism, stress response and especially, maturation as compared to their female counterparts.

INSTRUMENT(S): LTQ Orbitrap Velos

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Brain, Oligodendrocyte Precursor Cell

DISEASE(S): Mixed Disorder As Reaction To Stress

SUBMITTER: Elke Hammer  

LAB HEAD: Elke Hammer

PROVIDER: PXD011348 | Pride | 2021-09-08

REPOSITORIES: Pride

Dataset's files

Source:
Action DRS
161123_OV4_UL_Neo_C_3_F_1.mzXML Mzxml
161123_OV4_UL_Neo_C_3_F_1.pep.xml Pepxml
161123_OV4_UL_Neo_C_3_F_1.raw Raw
161123_OV4_UL_Neo_C_3_F_2.mzXML Mzxml
161123_OV4_UL_Neo_C_3_F_2.pep.xml Pepxml
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Publications

Nup133 and ERα mediate the differential effects of hyperoxia-induced damage in male and female OPCs.

Sunny Donna Elizabeth DE   Hammer Elke E   Strempel Sebastian S   Joseph Christy C   Manchanda Himanshu H   Ittermann Till T   Hübner Stephanie S   Weiss Frank Ulrich FU   Völker Uwe U   Heckmann Matthias M  

Molecular and cellular pediatrics 20200825 1


<h4>Background</h4>Hyperoxia is a well-known cause of cerebral white matter injury in preterm infants with male sex being an independent and critical risk factor for poor neurodevelopmental outcome. Sex is therefore being widely considered as one of the major decisive factors for prognosis and treatment of these infants. But unfortunately, we still lack a clear view of the molecular mechanisms that lead to such a profound difference. Hence, using mouse-derived primary oligodendrocyte progenitor  ...[more]

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