Article
A novel type of glial cell in the retina is stimulated by insulin-like growth factor 1 and may exacerbate damage to neurons and Müller glia.
Department of Neuroscience, The Ohio State University, College of Medicine, Columbus, OH 43210-1239, USA.
Glia (impact factor:
4.82).
11/2009;
58(6):633-49.
DOI:10.1002/glia.20950
pp.633-49
Source: PubMed
-
Article: Control of oligodendrocyte differentiation by the Nkx2.2 homeodomain transcription factor.
[show abstract] [hide abstract]
ABSTRACT: Oligodendrocytes are derived from glial precursors that arise from the ventral neural tube early in development. In the developing chicken CNS, oligodendrocyte progenitors selectively express Nkx2.2 homeodomain transcription factor, raising the possibility that Nkx2.2 may directly regulate oligogliogenesis. In this study, we have examined Nkx2.2 expression in rodent glial precursors and studied the effect of a loss of Nkx2.2 on oligodendrocyte and astrocyte differentiation. We show that Nkx2.2 is also expressed in mammalian oligodendrocyte progenitors and that the differentiation of MBP-positive and PLP-DM20-positive oligodendrocytes is dramatically retarded in Nkx2.2-null mutants along the entire rostrocaudal axis. In contrast, no effect is seen on astrocytic differentiation. Interestingly, absence of Nkx2.2 expression leads to a ventral expansion of the Olig1/Olig2 expression in neuroepithelial cells into the Nkx2.2 domain and a consequent increase in the production of Olig1/Olig2-positive and platelet-derived growth factor receptor alpha-positive oligodendrocyte progenitors. These results strongly suggest that Nkx2.2 regulates the differentiation and/or maturation, but not the initial specification, of oligodendrocyte progenitors. Consistent with this suggestion, overproduction of Nkx2.2 protein in fibroblast cells can induce gene expression from the proteolipid protein promoter.Development 08/2001; 128(14):2723-33. · 6.60 Impact Factor -
Article: Cell death in the nervous system: lessons from insulin and insulin-like growth factors.
[show abstract] [hide abstract]
ABSTRACT: Programmed cell death is an essential process for proper neural development. Cell death, with its similar regulatory and executory mechanisms, also contributes to the origin or progression of many or even all neurodegenerative diseases. An understanding of the mechanisms that regulate cell death during neural development may provide new targets and tools to prevent neurodegeneration. Many studies that have focused mainly on insulin-like growth factor-I (IGF-I), have shown that insulin-related growth factors are widely expressed in the developing and adult nervous system, and positively modulate a number of processes during neural development, as well as in adult neuronal and glial physiology. These factors also show neuroprotective effects following neural damage. Although some specific actions have been demonstrated to be anti-apoptotic, we propose that a broad neuroprotective role is the foundation for many of the observed functions of the insulin-related growth factors, whose therapeutical potential for nervous system disorders may be greater than currently accepted.Molecular Neurobiology 09/2003; 28(1):23-50. · 5.74 Impact Factor
Data provided are for informational purposes only. Although carefully collected, accuracy cannot be guaranteed.
The impact factor represents a rough estimation of the journal's impact factor and does not reflect the actual
current impact factor.
Publisher conditions are provided by RoMEO. Differing provisions from the publisher's actual policy or licence
agreement may be applicable.
Keywords
acute damage
avian retina
cell death
cells nonastrocytic inner retinal glia-like
detachment coinciding
distinct cell-type
excitotoxic damage
express Sox2
ganglion cell
glial cell
glial cells
IGF1 receptor
inner plexiform layers
insulin-like growth factor 1
known types
NIRG cells
numerous focal detachments
unique immunohistochemical profile
upregulate lysosomal membrane glycoprotein
upregulating transitin