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DOI 10.1016/j.neuroscience.2019.01.041

Медицинская библиотека · Neuroscience · 2019

Neurotrophic Factors and Their Receptors Are Altered by the Mere Partial IGF-1 Deficiency.

Castilla-Cortázar Inma, Iturrieta Ignacio, García-Magariño Mariano, Puche Juan E, Martín-Estal Irene, Aguirre Gabriel A, Femat-Roldan Giovana, Cantu-Martinez Leonel, Muñoz Úrsula

СтатьяПоддержка исследования: вне правительства СШАПеревод пока не подготовлен

Аннотация

Neurotrophic factors (NTFs) are a relevant group of secreted proteins that modulate growth, differentiation, repair, and survival of neurons, playing a role in the maintenance of the synaptic unions, dendrites, and axons and also being crucial for peripheral nervous system development and regulating plasticity in the adult central nervous system. On the other hand, insulin-like growth factor 1 (IGF-1) has been ascertained multiple beneficial actions in the brain: neuro-development, -protection, -genesis and plasticity. To further investigate the possible mechanisms underlying IGF-1 deficiency in the establishment of neurological disease, microarray and reverse transcription polymerase chain reaction gene expression analyses coupled with in silico processing were performed in an experimental model of partial IGF-1 deficiency. Results show that the mere IGF-1 deficiency seems to be responsible for an altered expression of genes coding for neurotrophic factors (particularly ciliary neurotrophic factor and mesencephalic astrocyte-derived neurotrophic factor), their receptors and signaling pathways (specially RET). The presented findings support that IGF-1 deficiency might be involved in the establishment and progression of neurodegenerative disorders.

Для цитирования: Castilla-Cortázar Inma, Iturrieta Ignacio, García-Magariño Mariano, Puche Juan E, Martín-Estal Irene, Aguirre Gabriel A, Femat-Roldan Giovana, Cantu-Martinez Leonel, Muñoz Úrsula. Neurotrophic Factors and Their Receptors Are Altered by the Mere Partial IGF-1 Deficiency.. Neuroscience. 2019. DOI: 10.1016/j.neuroscience.2019.01.041.

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