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Barreda-Manso, M. A.

Publications and source records attributed to Barreda-Manso, M. A..

3 recordsLinked to original sources

MiR-138-5p upregulation during neuronal maturation parallels with an increase in neuronal survival

Neuronal maturation is a process that plays a key role in the development and regeneration of the central nervous system. Although embryonic brain development and neurodegeneration have received considerable attention, the events that govern postnatal neuronal maturation are less understood. Among the mechanisms influencing such neuronal maturation process, apoptosis plays a key role. Several regulators have been described to modulate apoptosis, including post-transcriptional regulation by microRNAs. This study aimed to assess whether the strikingly induced miR-138-5p during neuronal maturation contributes to avoiding the neuronal death induced by apoptosis. Our results point out that the observed opposite expression of miR-138-5p and its target Caspase3 might modulate apoptosis favouring neuronal survival at distinct maturation stages. The unchanged expression of miR-138-5p in mature neurons contrasts with the significant downregulation in immature neurons upon apoptotic stimulation. Similarly, immunoblot and individual cellular assays confirmed that during maturation, not only the expression but processing of CASP-3 and caspase activity is reduced after apoptotic stimulation which resulted in a reduction of neuronal death. For all this data, we suggest that the upregulation of miR-138-5p during neuronal maturation is crucial in neuronal survival in pathological or traumatic conditions. Further studies would be needed to determine a more detailed role of miR-138-5p in apoptosis during neuronal maturation and the synergistic action of several microRNAs acting cooperatively on Caspase3 or other apoptotic targets. Graphical abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=166 SRC="FIGDIR/small/516547v2_ufig1.gif" ALT="Figure 1"> View larger version (47K): org.highwire.dtl.DTLVardef@e1eb95org.highwire.dtl.DTLVardef@31b0c9org.highwire.dtl.DTLVardef@4d895borg.highwire.dtl.DTLVardef@74c902_HPS_FORMAT_FIGEXP M_FIG C_FIG HighligthsO_LINeuronal maturation promotes cell survival. C_LIO_LINeuronal maturation reduces the processing of CASP-3 and caspase activity after apoptotic stimulation. C_LIO_LIThe expression changes of miR-138-5p and Caspase 3 are opposite during hippocampal neuron maturation. C_LIO_LIThe increase of miR-138-5p expression throughout maturation is not influenced by apoptotic stimulation. C_LIO_LIMiR-138-5p is suggested as an essential factor concerning neuronal maturation, regulating Caspase 3 and favouring survival. C_LI

neuroscience↗

STEREOLOGICAL EVALUATION OF TISSUE PRESERVATION AFTERNEUROPROTECTIVE TREATMENTS FOR TRAUMATIC SPINAL CORDINJURY

Spinal cord injury (SCI) is a major cause of permanent disability and its causes and pathophysiological effects are very variables between patients. The assessment of tissue damage extent and neurodegeneration degree correlated with the functional evaluation are the most accepted tools to diagnose and prognose the trauma severity. Animal models of SCI have been used for treatment development and in the present work we evaluate the potency of stereological tools to estimate damage degree for a diagnostic of neural degeneration and locomotor and sensorial disability after SCI and the efficacy of different types of therapeutic strategies.

neuroscience↗

MiR-182-5p regulates Nogo-A expression and promotes neurite outgrowth of hippocampal neurons in vitro

Nogo-A protein is a key myelin-associated inhibitor for axonal growth, regeneration, and plasticity in the central nervous system (CNS). Regulation of the Nogo-A/NgR1 pathway facilitates functional recovery and neural repair after spinal cord trauma and ischemic stroke. MicroRNAs are described as effective tools for the regulation of important processes in CNS such as neuronal differentiation, neuritogenesis, and plasticity. Our results showed that miR-182-5p mimic specifically downregulates the expression of the luciferase reporter gene fused to the mouse Nogo-A 3UTR, and Nogo-A protein expression in Neuro-2a and C6 cells. Finally, we observed that when rat primary hippocampal neurons are co-cultured with C6 cells transfected with miR-182-5p mimic, there is a promotion of the outgrowth of neuronal neurites in length. From all these data we suggest that miR-182-5p may be a potential therapeutic tool for the promotion of axonal regeneration in different diseases of the CNS. Graphical abstract O_FIG O_LINKSMALLFIG WIDTH=200 HEIGHT=78 SRC="FIGDIR/small/482803v1_ufig1.gif" ALT="Figure 1"> View larger version (17K): org.highwire.dtl.DTLVardef@e0979forg.highwire.dtl.DTLVardef@10265eborg.highwire.dtl.DTLVardef@71603dorg.highwire.dtl.DTLVardef@1654818_HPS_FORMAT_FIGEXP M_FIG C_FIG HighlightsO_LIBioinformatics analyses show that miR-182-5p targets Nogo-A 3UTR. C_LIO_LIMiR-182-5p downregulates Nogo-A protein expression in murine cell lines. C_LIO_LIMiR-182-5p promotes neurite outgrowth of rat primary hippocampal neurons in vitro. C_LIO_LIMiR-182-5p is suggested as a potential therapeutic tool for the promotion of axonal regeneration in different pathologies/diseases of the central nervous system. C_LI

neuroscience↗