Nerve growth factor-mediated vascular endothelial growth factor expression of astrocyte in retinal vascular development

Kim, You Sun; Jo, Dong Hyun; Lee, Hanjae; Kim, Jin Hyoung; Kim, Kyu Won; Kim, Jeong Hun

doi:10.1016/j.bbrc.2013.01.045

Cited by 21 publications

(12 citation statements)

References 31 publications

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“…Under physiological conditions, NGF and p75 NTR were mainly expressed in all cell types, while trkA NGFR was weakly expressed by RBCs and RGCs, in line with literature (Carmignoto et al 1991;Shi et al 2007;Kim et al 2013;Weng et al 2013). As second point, low Annexin V expression was detected in Reelin-deprived RGCs and RBCs.…”

Section: Discussionsupporting

confidence: 61%

NGF Expression in Reelin-Deprived Retinal Cells: A Potential Neuroprotective Effect

et al. 2015

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We recently reported that increased NGF and p75(NTR) as well as decreased trkA(NGFR) characterized the Reelin-deprived (E-Reeler) retina, prospecting a potential contribution of NGF during E-Reeler retinogenesis. Herein, retinal ganglion cells (RGCs), glial cells and rod bipolar cells (RBCs) were isolated from E-Reeler retinas, and NGF, trkA(NGFR)/p75(NTR) expression and apoptosis were investigated. E-Reeler (n = 28) and E-control (n = 34) retinas were digested, and RGCs, glial cells and RBCs were isolated by the magnetic bead separation. Expression of NGF, trkA(NGFR), p75(NTR), Annexin V/PI and Bcl2/Bax was quantified by flow cytometry and validated by real-time PCR or WB. In E-Reeler retinas, NGF was significantly increased in RGCs and glial cells, p75(NTR) was increased in both RBCs and RGCs, and trkA(NGFR) was unchanged. In E-control retinas, NGF and p75(NTR) were expressed mainly in RBCs and RGCs and faintly in glial cells, while trkA(NGFR) was weakly expressed by RBCs and RGCs. In RBCs and RGCs, Annexin V expression was unchanged, while Bcl2 increased and Bax decreased selectively in E-Reeler RGCs. The data indicate that E-Reeler RBCs and RGCs overexpress NGF and p75(NTR) as a protective endogenous response to Reelin deprivation. The observation is strongly supported by the absence of apoptosis in both cell types.

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Section: Discussionsupporting

confidence: 61%

NGF Expression in Reelin-Deprived Retinal Cells: A Potential Neuroprotective Effect

et al. 2015

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“…Indeed, NGF immunoreactivity was greatly expressed in accessory/glial cells, representing certainly the main NGF source in the damaged neighbourhood [29–32]. The observation of increased NGF protein, not corroborated by the molecular data, might be explained as possible transcriptional/posttranscriptional regulations (differential regulation, stability, and degradation of mRNA).…”

Section: Discussionmentioning

confidence: 99%

Characterization of NGF, trkA^NGFR, and p75^NTRin Retina of Mice Lacking Reelin Glycoprotein

Balzamino

Biamonte

Esposito

et al. 2014

International Journal of Cell Biology

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Both Reelin and Nerve Growth Factor (NGF) exert crucial roles in retinal development. Retinogenesis is severely impaired in E-reeler mice, a model of Reelin deficiency showing specific Green Fluorescent Protein expression in Rod Bipolar Cells (RBCs). Since no data are available on Reelin and NGF cross-talk, NGF and trkANGFR/ p75NTR expression was investigated in retinas from E-reeler versus control mice, by confocal microscopy, Western blotting, and real time PCR analysis. A scattered increase of NGF protein was observed in the Ganglion Cell Layer and more pronounced in the Inner Nuclear Layer (INL). A selective increase of p75NTR was detected in most of RBCs and in other cell subtypes of INL. On the contrary, a slight trend towards a decrease was detected for trkANGFR, albeit not significant. Confocal data were validated by Western blot and real time PCR. Finally, the decreased trkANGFR/ p75NTR ratio, representative of p75NTR increase, significantly correlated with E-reeler versus E-control. These data indicate that NGF-trkANGFR/ p75NTR is affected in E-reeler retina and that p75NTR might represent the main NGF receptor involved in the process. This first NGF-trkANGFR/ p75NTR characterization suggests that E-reeler might be suitable for exploring Reelin-NGF cross-talk, representing an additional information source in those pathologies characterized by retinal degeneration.

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“…Overexpression by electroporation of pro‐NGF plasmid in rat retinas increased BRB permeability, as assessed by the increased extravasation of plasma proteins (Matragoon et al., ). Furthermore, in vitro experiments in human retinal ECs revealed angiogenic functions of pro‐NGF when interacting with TrkA (Elshaer et al., ), and in vitro studies in astrocytes also demonstrated the ability of pro‐NGF to increase VEGF (Kim et al., ).…”

Section: Trophic Factorsmentioning

confidence: 99%

A journey into the retina: Müller glia commanding survival and death

Subirada

Paz

Ridano

et al. 2018

Eur J of Neuroscience

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Müller glial cells (MGCs) are known to participate actively in retinal development and to contribute to homoeostasis through many intracellular mechanisms. As there are no homologous cells in other neuronal tissues, it is certain that retinal health depends on MGCs. These macroglial cells are located at the centre of the columnar subunit and have a great ability to interact with neurons, astrocytes, microglia and endothelial cells in order to modulate different events. Several investigations have focused their attention on the role of MGCs in diabetic retinopathy, a progressive pathology where several insults coexist. As expected, data suggest that MGCs display different responses according to the severity of the stimulus, and therefore trigger distinct events throughout the course of the disease. Here, we describe physiological functions of MGCs and their participation in inflammation, gliosis, synthesis and secretion of trophic and antioxidant factors in the diabetic retina. We invite the reader to consider the protective/deleterious role of MGCs in the early and late stages of the disease. In the light of the results, we open up the discussion around and ask the question: Is it possible that the modulation of a single cell type could improve or even re-establish retinal function after an injury?

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Nerve growth factor-mediated vascular endothelial growth factor expression of astrocyte in retinal vascular development

Cited by 21 publications

References 31 publications

NGF Expression in Reelin-Deprived Retinal Cells: A Potential Neuroprotective Effect

NGF Expression in Reelin-Deprived Retinal Cells: A Potential Neuroprotective Effect

Characterization of NGF, trkA^NGFR, and p75^NTRin Retina of Mice Lacking Reelin Glycoprotein

A journey into the retina: Müller glia commanding survival and death

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Nerve growth factor-mediated vascular endothelial growth factor expression of astrocyte in retinal vascular development

Cited by 21 publications

References 31 publications

NGF Expression in Reelin-Deprived Retinal Cells: A Potential Neuroprotective Effect

NGF Expression in Reelin-Deprived Retinal Cells: A Potential Neuroprotective Effect

Characterization of NGF, trkANGFR, and p75NTRin Retina of Mice Lacking Reelin Glycoprotein

A journey into the retina: Müller glia commanding survival and death

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Characterization of NGF, trkA^NGFR, and p75^NTRin Retina of Mice Lacking Reelin Glycoprotein