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Endogenous erythropoietin signaling regulates migration and laminar positioning of upper-layer neurons in the developing neocortex.

Development (Cambridge, England) (2020-08-09)
Paul E Constanthin, Alessandro Contestabile, Volodymyr Petrenko, Charles Quairiaux, Patrick Salmon, Petra S Hüppi, Jozsef Z Kiss
ABSTRAKT

Erythropoietin (EPO), the hypoxia-inducible hematopoietic hormone, has well-established neuroprotective/neurotrophic roles in the developing central nervous system and the therapeutic potential of EPO has been widely explored in clinical studies for the treatment of perinatal hypoxic brain lesion, as well as prematurity. Here, we reveal that both EPO and Epo receptor (EPOR) are expressed in the developing rat somatosensory cortex during radial migration and laminar positioning of granular and supragranular neurons. Experimental deregulation of EPO signaling using genetic approaches results in aberrant migration, as well as permanent neuronal misplacement leading to abnormal network activity and protracted sensory behavioral deficits. We identify ERK as the downstream effector of the EPO signaling pathway for neuronal migration. These findings reveal a crucial role for endogenous EPO signaling in neuronal migration, and offer important insights for understanding how the temporary deregulation of EPO could result in migration defects that lead to abnormal behavior in the adult.

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Sigma-Aldrich
Anti-Nestin Antibody, clone rat-401, clone rat-401, Chemicon®, from mouse
Sigma-Aldrich
Anti-EPO-R antibody produced in rabbit, affinity isolated antibody
Sigma-Aldrich
Sodium phosphate monobasic solution, BioUltra, 5 M in H2O
Sigma-Aldrich
Anti-NeuN Antibody, clone A60, clone A60, Chemicon®, from mouse