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• W2056594163 abstract "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<mml:math xmlns:mml=http://www.w3.org/1998/Math/MathML id=M1><mml:mrow><mml:msup><mml:mrow><mml:mtext>trkA</mml:mtext></mml:mrow><mml:mrow><mml:mtext>NGFR</mml:mtext></mml:mrow></mml:msup></mml:mrow></mml:math>/<mml:math xmlns:mml=http://www.w3.org/1998/Math/MathML id=M2><mml:mtext>p</mml:mtext><mml:msup><mml:mrow><mml:mtext>75</mml:mtext></mml:mrow><mml:mrow><mml:mtext>NTR</mml:mtext></mml:mrow></mml:msup></mml:math>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<mml:math xmlns:mml=http://www.w3.org/1998/Math/MathML id=M3><mml:mtext>p</mml:mtext><mml:msup><mml:mrow><mml:mtext>75</mml:mtext></mml:mrow><mml:mrow><mml:mtext>NTR</mml:mtext></mml:mrow></mml:msup></mml:math>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<mml:math xmlns:mml=http://www.w3.org/1998/Math/MathML id=M4><mml:mrow><mml:msup><mml:mrow><mml:mtext>trkA</mml:mtext></mml:mrow><mml:mrow><mml:mtext>NGFR</mml:mtext></mml:mrow></mml:msup></mml:mrow></mml:math>, albeit not significant. Confocal data were validated by Western blot and real time PCR. Finally, the decreased<mml:math xmlns:mml=http://www.w3.org/1998/Math/MathML id=M5><mml:mrow><mml:msup><mml:mrow><mml:mtext>trkA</mml:mtext></mml:mrow><mml:mrow><mml:mtext>NGFR</mml:mtext></mml:mrow></mml:msup></mml:mrow></mml:math>/<mml:math xmlns:mml=http://www.w3.org/1998/Math/MathML id=M6><mml:mtext>p</mml:mtext><mml:msup><mml:mrow><mml:mtext>75</mml:mtext></mml:mrow><mml:mrow><mml:mtext>NTR</mml:mtext></mml:mrow></mml:msup></mml:math>ratio, representative of<mml:math xmlns:mml=http://www.w3.org/1998/Math/MathML id=M7><mml:mtext>p</mml:mtext><mml:msup><mml:mrow><mml:mtext>75</mml:mtext></mml:mrow><mml:mrow><mml:mtext>NTR</mml:mtext></mml:mrow></mml:msup></mml:math>increase, significantly correlated with E-reeler versus E-control. These data indicate that NGF-<mml:math xmlns:mml=http://www.w3.org/1998/Math/MathML id=M8><mml:mrow><mml:msup><mml:mrow><mml:mtext>trkA</mml:mtext></mml:mrow><mml:mrow><mml:mtext>NGFR</mml:mtext></mml:mrow></mml:msup></mml:mrow></mml:math>/<mml:math xmlns:mml=http://www.w3.org/1998/Math/MathML id=M9><mml:mtext>p</mml:mtext><mml:msup><mml:mrow><mml:mtext>75</mml:mtext></mml:mrow><mml:mrow><mml:mtext>NTR</mml:mtext></mml:mrow></mml:msup></mml:math>is affected in E-reeler retina and that<mml:math xmlns:mml=http://www.w3.org/1998/Math/MathML id=M10><mml:mtext>p</mml:mtext><mml:msup><mml:mrow><mml:mtext>75</mml:mtext></mml:mrow><mml:mrow><mml:mtext>NTR</mml:mtext></mml:mrow></mml:msup></mml:math>might represent the main NGF receptor involved in the process. This first NGF-<mml:math xmlns:mml=http://www.w3.org/1998/Math/MathML id=M11><mml:mrow><mml:msup><mml:mrow><mml:mtext>trkA</mml:mtext></mml:mrow><mml:mrow><mml:mtext>NGFR</mml:mtext></mml:mrow></mml:msup></mml:mrow></mml:math>/<mml:math xmlns:mml=http://www.w3.org/1998/Math/MathML id=M12><mml:mtext>p</mml:mtext><mml:msup><mml:mrow><mml:mtext>75</mml:mtext></mml:mrow><mml:mrow><mml:mtext>NTR</mml:mtext></mml:mrow></mml:msup></mml:math>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." @default.
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• W2056594163 date "2014-01-01" @default.
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• W2056594163 title "Characterization of NGF, trkA^<b>NGFR</b>, and p75^<b>NTR</b>in Retina of Mice Lacking Reelin Glycoprotein" @default.
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• W2056594163 doi "https://doi.org/10.1155/2014/725928" @default.
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