Correction to: Role of astrocytic MeCP2 in regulation of CNS myelination by affecting oligodendrocyte and neuronal physiology and axo–glial interactions

Differential brain region‐specific expression of MeCP2 and BDNF in Rett Syndrome patients: a distinct grey‐white matter variation

“…In the absence of obvious change in the MBP and without labelling with an astrocyte nuclear marker, it is not fully clear whether the astrocyte number or the GFAP production is reduced. Regardless, these data support prior studies, mainly in animal models, by suggesting an important role for glial dysfunction in human RTT brain [70‐73].…”

Glial Dysfunction in MeCP2 Deficiency Models: Implications for Rett Syndrome

“…Similarly, astrocytes derived from human RTT iPSCs and the ACM from these cells also have an adverse effect on WT mouse neurons [69]. Finally, ACM from Mecp2 -siRNA-treated primary astrocytes induces reduced neuronal viability in WT dorsal root ganglion neurons [70]. These aberrant neurons also show significant functional changes.…”

“…Apart from supporting neurons, astrocytes also facilitate oligodendrocyte function by releasing growth factors that promote their differentiation from oligodendrocyte precursor cells (OPCs), promote maturation, and promote expression of genes that are involved in myelination [74]. ACM from Mecp2 -siRNA-treated KD astrocyte cultures exerted a negative effect on OPC proliferation, and when mature oligodendrocytes were co-cultured with KD astrocytes, proteins associated with myelination, such as MBP and PLP, were downregulated [70]. Historically, the neuron-glia interaction has been a focus of interest in understanding the role of typical and dysfunctional astrocyte contribution to health.…”

“…On the other hand, Mecp2 deficiency in astrocytes cultured from both Mecp2 tm1.1Bird/y and Mecp2 tm1.1Jae/y causes an increase in Bdnf transcription [15], in line with astrocyte reactivity in RTT. A different study that used astrocytic primary cultures from rats found that Mecp2 KD astrocytes express more, but secrete less, Bdnf [70]. Remarkably, neurons from Mecp 308/y mice had more Bdnf VI transcript, but not in astrocytes [92].…”

“…In contrast, Mecp2 -mutated neuronal progenitor cells showed decreased oligodendrocyte differentiation [118]. Another siRNA co-culture model showed that Nf155 , a gene associated with axo-glial interactions, is decreased in Mecp2 KD oligodendrocytes, while the axo-glial genes Caspr and Nrl1 are upregulated in Mecp2 KD neurons [70]. Therefore, it appears that Mecp2 uniquely regulates neuron-oligodendrocyte communication in a cell-specific manner.…”