Role of adherens junctions and apical-basal polarity of neural stem/progenitor cells in the pathogenesis of neurodevelopmental disorders: a novel perspective on congenital Zika syndrome

Felipe A. Bustamante, MarÍa Paz Miró, Zahady D. VelÁsquez, Luis Molina, Pamela Ehrenfeld, Francisco J. Rivera, Luis Federico Batiz

Research output: Contribution to journalReview articlepeer-review

4 Scopus citations

Abstract

Radial glial cells (RGCs) are the neural stem/progenitor cells (NSPCs) that give rise to most of neurons and glial cells that constitute the adult central nervous system. A hallmark of RGCs is their polarization along the apical-basal axis. They extend a long basal process that contacts the pial surface and a short apical process to the ventricular surface. Adherens junctions (AJs) are organized as belt-like structures at the most-apical lateral plasma membrane of the apical processes. These junctional complexes anchor RGCs to each other and allow the recruitment of cytoplasmic proteins that act as apical-basal determinants. It has been proposed that disruption of AJs underlies the onset of different neurodevelopmental disorders. In fact, studies performed in different animal models indicate that loss of function of AJs-related proteins in NSPCs can disrupt cell polarity, imbalance proliferation and/or differentiation rates and increase cell death, which, in turn, lead to disruption of the cytoarchitecture of the ventricular zone, protrusion of non-polarized cells into the ventricles, cortical thinning, and ventriculomegaly/hydrocephalus, among other neuropathological findings. Recent Zika virus (ZIKV) outbreaks and the high comorbidity of ZIKV infection with congenital neurodevelopmental defects have led to the World Health Organization to declare a public emergency of international concern. Thus, noteworthy advances have been made in clinical and experimental ZIKV research. This review summarizes the current knowledge regarding the function of AJs in normal and pathological corticogenesis and focuses on the neuropathological and cellular mechanisms involved in congenital ZIKV syndrome, highlighting the potential role of cell-to-cell junctions between NSPCs in the etiopathogenesis of such syndrome.

Original languageEnglish
Pages (from-to)57-79
Number of pages23
JournalTranslational Research
Volume210
DOIs
StatePublished - Aug 2019

Bibliographical note

Funding Information:
All authors have read the journal's policy on disclosure of potential conflicts of interest. All authors have disclosed any financial or personal relationship with organizations that could potentially be perceived as influencing the described research. All authors have declared that no potential conflict of interest exists. All authors have read the journal's authorship agreement and the manuscript has been reviewed by and approved by all named authors. The authors acknowledge the support of Carlos Figueroa (UACh), Lara Jorge Monteiro and Mar?a Teresa Valenzuela (UAndes). This work was supported in part by Chilean FONDECYT Regular Grant 1141015 (LFB), Chilean FONDECYT Regular Grant 1161787 (FJR), Chilean FONDECYT Postdoctoral Grant 3130756 (ZDV), and Chilean CONICYT Doctoral Scholarship 21160084 (FAB).

Funding Information:
The authors acknowledge the support of Carlos Figueroa (UACh), Lara Jorge Monteiro and María Teresa Valenzuela (UAndes). This work was supported in part by Chilean FONDECYT Regular Grant 1141015 (LFB), Chilean FONDECYT Regular Grant 1161787 (FJR), Chilean FONDECYT Postdoctoral Grant 3130756 (ZDV), and Chilean CONICYT Doctoral Scholarship 21160084 (FAB).

Publisher Copyright:
© 2019 Elsevier Inc.

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