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通过Na1.5通道鉴定钠瞬变作为永生化背根神经节神经元分化的调节因子。

Identification of Sodium Transients Through Na1.5 Channels as Regulators of Differentiation in Immortalized Dorsal Root Ganglia Neurons.

作者信息

Martínez Antón L, Brea José, Domínguez Eduardo, Varela María J, Allegue Catarina, Cruz Raquel, Monroy Xavier, Merlos Manuel, Burgueño Javier, Carracedo Ángel, Loza María Isabel

机构信息

BioFarma Research Group, Centro Singular de Investigación en Medicina Molecular y Enfermedades Crónicas (CIMUS), Universidade de Santiago de Compostela, Santiago de Compostela, Spain.

Grupo de Medicina Xenómica, Centro de Investigación Biomédica en Red de Enfermedades Raras (CIBERER), Universidade de Santiago de Compostela, Santiago de Compostela, Spain.

出版信息

Front Cell Neurosci. 2022 Apr 6;16:816325. doi: 10.3389/fncel.2022.816325. eCollection 2022.

DOI:10.3389/fncel.2022.816325
PMID:35465610
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC9018981/
Abstract

Neuronal differentiation is a complex process through which newborn neurons acquire the morphology of mature neurons and become excitable. We employed a combination of functional and transcriptomic approaches to deconvolute and identify key regulators of the differentiation process of a DRG neuron-derived cell line, and we focused our study on the Na 1.5 ion channel (encoded by ) as a channel involved in the acquisition of DRG neuronal features. Overexpression of enhances the acquisition of neuronal phenotypic features and increases the KCl-elicited hyperexcitability response in a DRG-derived cell line. Moreover, pharmacologic inhibition of the Na 1.5 channel during differentiation hinders the acquisition of phenotypic features of neuronal cells and the hyperexcitability increase in response to changes in the extracellular medium ionic composition. Taken together, these data highlight the relevance of sodium transients in regulating the neuronal differentiation process in a DRG neuron-derived cell line.

摘要

神经元分化是一个复杂的过程，新生神经元通过这个过程获得成熟神经元的形态并变得可兴奋。我们采用功能和转录组学方法相结合的方式，对背根神经节（DRG）神经元衍生细胞系分化过程的关键调节因子进行解卷积和鉴定，并将研究重点放在Na 1.5离子通道（由[具体基因名称]编码）上，该通道参与DRG神经元特征的获得。[具体基因名称]的过表达增强了神经元表型特征的获得，并增加了DRG衍生细胞系中氯化钾引发的过度兴奋反应。此外，在分化过程中对Na 1.5通道进行药理抑制会阻碍神经元细胞表型特征的获得以及对细胞外培养基离子组成变化的过度兴奋增加。综上所述，这些数据突出了钠瞬变在调节DRG神经元衍生细胞系神经元分化过程中的相关性。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2abf/9018981/ff25f16d177f/fncel-16-816325-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2abf/9018981/1ec4ec531dd6/fncel-16-816325-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2abf/9018981/e96648295cc5/fncel-16-816325-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2abf/9018981/7c0336d3411d/fncel-16-816325-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2abf/9018981/ff25f16d177f/fncel-16-816325-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2abf/9018981/1ec4ec531dd6/fncel-16-816325-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2abf/9018981/e96648295cc5/fncel-16-816325-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2abf/9018981/7c0336d3411d/fncel-16-816325-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2abf/9018981/ff25f16d177f/fncel-16-816325-g004.jpg

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