Glial fibrillary acidic protein‐expressing cells in the neurogenic regions in normal and injured adult brains

Zhu, Hong; Dahlström, Annica

doi:10.1002/jnr.21257

Cited by 27 publications

(19 citation statements)

References 62 publications

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“…This antibody stains neural stem cells in the neurogenic regions, the SVZ, and the subgranular zone of the dentate gyrus (Doetsch et al, 1999;Morshead et al, 2003;Zhu and Dahlström, 2007;Ihrie and Alvarez-Buylla, 2008), which is comparable to our results.…”

Section: Antibody Characterizationsupporting

confidence: 93%

Expression of vascular endothelial growth factor receptor‐3 mRNA in the rat developing forebrain and retina

Choi

Shin

Lee

et al. 2010

J of Comparative Neurology

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Vascular endothelial growth factor receptor (VEGFR)-3, a receptor for VEGF-C and VEGF-D, is expressed in neural progenitor cells, but there has been no comprehensive study of its distribution in the developing brain. Here, the temporal and cell-specific expression of VEGFR-3 mRNA was studied in the developing rat forebrain and eye. Expression appeared along the ventricular and subventricular zones of the lateral and third ventricles showing ongoing neurogenesis as early as embryonic day 13 but was progressively down-regulated during development and remained in the subventricular zone and rostral migratory stream of the adult forebrain. VEGFR-3 expression was also detectable in some differentiating and postmitotic neurons in the developing cerebral cortex, including Cajal-Retzius cells, cortical plate neurons, and subplate neurons. Expression in the subplate increased significantly during the early postnatal period but was absent by postnatal day 14. It was also highly expressed in nonneural tissues of the eye during development, including the retinal pigment epithelium, the retinal ciliary margin, and the lens, but persisted in a subset of cells in the pigmented ciliary epithelium of the adult eye. In contrast, there was weak or undetectable expression in the early neural retina, but a subset of retinal neurons in the postnatal and mature retina showed intense signals. These unique spatiotemporal mRNA expression patterns suggest that VEGFR-3 might mediate the regulation of both neurogenesis and adult neuronal function in the rat forebrain and eye.

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Section: Antibody Characterizationsupporting

confidence: 93%

Expression of vascular endothelial growth factor receptor‐3 mRNA in the rat developing forebrain and retina

Choi

Shin

Lee

et al. 2010

J of Comparative Neurology

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“…This was in sharp contrast to our observation in undifferentiated NPCs, where GFAP mRNA levels decreased 100-fold as early as 24 h p.i., with protein declines beginning at 48 h p.i. This suggested that GFAP's function and/or regulation was considerably different in NPCs than in astroglia, which has been suggested by others (80). In our experiments, changes to attachment and spreading characteristics observed during infection of neurospheres paralleled those seen during astroglial differentiation.…”

Section: Discussionsupporting

confidence: 82%

Human Cytomegalovirus Infection Causes Premature and Abnormal Differentiation of Human Neural Progenitor Cells

Luo

Hannemann

Kulkarni

et al. 2010

J Virol

101

162

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Congenital human cytomegalovirus (HCMV) infection is a leading cause of birth defects, largely manifested as central nervous system (CNS) disorders. The principal site of manifestations in the mouse model is the fetal brain's neural progenitor cell (NPC)-rich subventricular zone. Our previous human NPC studies found these cells to be fully permissive for HCMV and a useful in vitro model system. In continuing work, we observed that under culture conditions favoring maintenance of multipotency, infection caused NPCs to quickly and abnormally differentiate. This phenotypic change required active viral transcription. Whole-genome expression analysis found rapid downregulation of genes that maintain multipotency and establish NPCs' neural identity. Quantitative PCR, Western blot, and immunofluorescence assays confirmed that the mRNA and protein levels of four hallmark NPC proteins (nestin, doublecortin, sex-determining homeobox 2, and glial fibrillary acidic protein) were decreased by HCMV infection. The decreases required active viral replication and were due, at least in part, to proteasomal degradation. Our results suggest that HCMV infection causes in utero CNS defects by inducing both premature and abnormal differentiation of NPCs.Congenital human cytomegalovirus (HCMV) infection is a leading cause of birth defects, primarily affecting the central nervous system (CNS). Primary infection during pregnancy poses a 30 to 40% risk of intrauterine transmission, with severe adverse outcomes more likely if the infection occurs within the first half of gestation (46). Each year, approximately 1% of all newborns are congenitally infected with HCMV. Approximately 5 to 10% of these infants manifest signs of serious neurological defects at birth, including deafness, mental retardation, blindness, microencephaly, hydrocephalus, and cerebral calcification (2,4,65). In addition, 10 to 15% of congenitally infected infants who are asymptomatic at birth subsequently develop brain disorders such as sensorineural hearing loss (12, 47, 52). Moreover, accumulating evidence suggests that more subtle changes in human brain development, such as autism and language development, may be related to congenital HCMV infection (68,76,77).Although HCMV can infect a wide range of tissues in vivo (61), the fetal brain is the principal site of the deleterious manifestations of infection. It has been suggested that the severity of neuropathological changes and clinical outcomes may be associated with the stage of CNS development at which congenital infection occurs, with early-gestation infections producing more severe outcomes (3, 46). However, the mechanism of HCMV pathogenesis in the developing CNS remains poorly understood. Studies of HCMV in human subjects have obvious limitations; therefore, model systems of both in vitro and in vivo HCMV infections have been devised to provide insights into infection of the developing brain.Congenital infection studies have been performed principally with the mouse model. Studies of mice revealed that very ea...

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“…To confirm the multipotency of accumulated cells, isolated cells from six mice in the treated and untreated injured groups were pooled, expanded to 70% confluence, and evaluated for their ability to differentiate along ectodermal and mesodermal lineages in vitro. Following culture in conditions of neuroectodermal differentiation, cells from ECM treated mice showed heterogeneous morphologies including spindle-like cells with long processes that expressed β3-tubulin and NeuN, markers of differentiating neurons (26), and stellate shaped cells that expressed glial fibrillary acidic protein (GFAP), a marker of glial cells that is also expressed by some neural stem cells (27,28) (Fig. 3).…”

Section: Ecm Degradation Products Promote the Accumulation Of Mononucmentioning

confidence: 99%

Epimorphic regeneration approach to tissue replacement in adult mammals

Agrawal

Johnson²,

Reing³

et al. 2009

Proc. Natl. Acad. Sci. U.S.A.

141

134

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Urodeles and fetal mammals are capable of impressive epimorphic regeneration in a variety of tissues, whereas the typical default response to injury in adult mammals consists of inflammation and scar tissue formation. One component of epimorphic regeneration is the recruitment of resident progenitor and stem cells to a site of injury. Bioactive molecules resulting from degradation of extracellular matrix (ECM) have been shown to recruit a variety of progenitor and stem cells in vitro in adult mammals. The ability to recruit multipotential cells to the site of injury by in vivo administration of chemotactic ECM degradation products in a mammalian model of digit amputation was investigated in the present study. Adult, 6- to 8-week-old C57/BL6 mice were subjected to midsecond phalanx amputation of the third digit of the right hind foot and either treated with chemotactic ECM degradation products or left untreated. At 14 days after amputation, mice treated with ECM degradation products showed an accumulation of heterogeneous cells that expressed markers of multipotency, including Sox2, Sca1, and Rex1 (Zfp42). Cells isolated from the site of amputation were capable of differentiation along neuroectodermal and mesodermal lineages, whereas cells isolated from control mice were capable of differentiation along only mesodermal lineages. The present findings demonstrate the recruitment of endogenous stem cells to a site of injury, and/or their generation/proliferation therein, in response to ECM degradation products.

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Glial fibrillary acidic protein‐expressing cells in the neurogenic regions in normal and injured adult brains

Cited by 27 publications

References 62 publications

Expression of vascular endothelial growth factor receptor‐3 mRNA in the rat developing forebrain and retina

Expression of vascular endothelial growth factor receptor‐3 mRNA in the rat developing forebrain and retina

Human Cytomegalovirus Infection Causes Premature and Abnormal Differentiation of Human Neural Progenitor Cells

Epimorphic regeneration approach to tissue replacement in adult mammals

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