Expression of glial fibrillary acidic protein in primary cultures of human Müller cells

Lupien, C.; Brenner, Michael; Guérin, Sylvain L.; Salesse, Christian

doi:10.1016/j.exer.2004.05.008

Cited by 22 publications

(16 citation statements)

References 37 publications

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“…4, compared with that in the non-injury side, GFAP proteins were also increased in injured DRG at two-days and two-weeks post nerve injury, which returned to a level close to that observed in non-injured DRG 20-weeks post nerve injury. The two protein bands detected were identical to the reported GFAP protein band pattern in Western blots in which the upper band matched the size of expected intact GFAP proteins, and the lower band represented presumably degradation product [31]. The pattern of increased GFAP protein expression, however, differed from that of GFAP mRNA.…”

Section: Resultssupporting

confidence: 72%

Profiling of dynamically changed gene expression in dorsal root ganglia post peripheral nerve injury and a critical role of injury-induced glial fibrillary acetic protein in maintenance of pain behaviors

Kim

Figueroa

et al. 2009

Pain

106

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To explore cellular changes in sensory neurons after nerve injury and identify potential target genes contributing to different stages of neuropathic pain development, we used Affymetrix oligo arrays to profile gene expression patterns in L5/6 dorsal root ganglia (DRG) from the neuropathic pain model of left L5/6 spinal nerve ligation at different stages of neuropathic pain development. Our data indicated that nerve injury induced changes in expression of genes with similar biological functions in a temporal specific manner that correlates with particular stages of neuropathic pain development, indicating dynamic neuroplasticity in the DRG in response to peripheral nerve injury and during neuropathic pain development. Data from post-array validation indicated that there was a temporal correlation between injury-induced expression of the glial fibrillary acidic protein (GFAP), a marker for activated astrocytes, and neuropathic pain development. Spinal nerve ligation injury in GFAP knockout mice resulted in neuropathic pain states with similar onset, but a shortened duration compared with that in age, and gender-matched wild-type littermates. Intrathecal GFAP antisense oligonucleotide treatment in injured rats with neuropathic pain states reversed injury-induced behavioral hypersensitivity and GFAP upregulation in DRG and spinal cord. Together, these findings indicate that injury-induced GFAP upregulation not only serves as a marker for astrocyte activation, but it may play a critical, but yet identified, role in the maintenance of neuropathic pain states.

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Section: Resultssupporting

confidence: 72%

Profiling of dynamically changed gene expression in dorsal root ganglia post peripheral nerve injury and a critical role of injury-induced glial fibrillary acetic protein in maintenance of pain behaviors

Kim

Figueroa

et al. 2009

Pain

106

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“…In the retina, Müller glia express low levels of Gfap in the absence of injury or disease, whereas retinal astrocytes constitutively express high levels of Gfap. 47 Consistent with this, the SAGE tag ratio of vimentin to Gfap in two human Müller glial cell lines was 164:1 48 ; by immunohistochemistry, human Müller glial cell lines 21 and primary rat Müller glial cultures 31 also expressed very low levels of GFAP. In contrast to ImM10 and C57M10 cells, mouse Müller cells (mMCI and mMCII) cultured from P5 to 12 mice express high levels of Gfap and low levels vimentin by RT-PCR.…”

Section: Discussionsupporting

confidence: 52%

“…Müller glial cell lines from multiple species have been generated from a variety of ages by both spontaneous immortalization and overexpression of viral oncogenes. 11,19,21,24,48 This likely reflects the inherent proliferative ability of Müller glia in vivo and potentially the limited stem cell-like properties of some Müller glia, both in vivo and in vitro. 10 We conclude that the morphologic and gene expression profiles of the ImM10 and C57M10 cell lines are consistent with their identification as Müller glia.…”

Section: Discussionmentioning

confidence: 99%

A Conditional Immortalized Mouse Müller Glial Cell Line Expressing Glial and Retinal Stem Cell Genes

Otteson

Phillips

2010

Invest. Ophthalmol. Vis. Sci.

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“…Up‐regulation of GFAP, an intermediate filament protein, is commonly used as a hallmark for reactive gliosis in models of retinal degeneration including RP (25, 26). Both Müller glial cells and astrocytes express GFAP under pathologic conditions (27, 28). GFAP was up‐regulated in retinas of rd10 mice from P18 to ‐60 ( P < 0.001, Mann–Whitney U test) compared with control retinas, the highest value being found at P30 (Fig.…”

Section: Resultsmentioning

confidence: 99%

HIF‐1α stabilization reduces retinal degeneration in a mouse model of retinitis pigmentosa

et al. 2018

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Retinitis pigmentosa (RP) is a group of inherited retinal dystrophies characterized by progressive and irreversible loss of vision due to rod and cone degeneration. Evidence suggests that an inappropriate oxygen level could contribute to its pathogenesis. Rod cell death could increase oxygen concentration, reduce hypoxia-inducible factor 1 (HIF-1α) and contribute to cone cell death. The purposes of this study were: 1) to analyze the temporal profile of HIF-1α, its downstream effectors VEGF, endothelin-1 (ET-1), iNOS, and glucose transporter 1 (GLUT1), and neuroinflammation in retinas of the murine model of rd10 ( retinal degeneration 10) mice with RP; 2) to study oxygen bioavailability in these retinas; and 3) to investigate how stabilizing HIF-1α proteins with dimethyloxaloglycine (DMOG), a prolyl hydroxylase inhibitor, affects retinal degeneration, neuroinflammation, and antioxidant response in rd10 mice. A generalized down-regulation of HIF-1α and its downstream targets was detected in parallel with reactive gliosis, suggesting high oxygen levels during retinal degeneration. At postnatal d 18, DMOG treatment reduced photoreceptor cell death and glial activation. In summary, retinas of rd10 mice seem to be exposed to a hyperoxic environment even at early stages of degeneration. HIF-1α stabilization could have a temporal neuroprotective effect on photoreceptor cell survival, glial activation, and antioxidant response at early stages of RP.-Olivares-González, L., Martínez-Fernández de la Cámara, C., Hervás, D., Millán, J. M., Rodrigo, R. HIF-1α stabilization reduces retinal degeneration in a mouse model of retinitis pigmentosa.

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Expression of glial fibrillary acidic protein in primary cultures of human Müller cells

Cited by 22 publications

References 37 publications

Profiling of dynamically changed gene expression in dorsal root ganglia post peripheral nerve injury and a critical role of injury-induced glial fibrillary acetic protein in maintenance of pain behaviors

Profiling of dynamically changed gene expression in dorsal root ganglia post peripheral nerve injury and a critical role of injury-induced glial fibrillary acetic protein in maintenance of pain behaviors

A Conditional Immortalized Mouse Müller Glial Cell Line Expressing Glial and Retinal Stem Cell Genes

HIF‐1α stabilization reduces retinal degeneration in a mouse model of retinitis pigmentosa

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