TY - JOUR
T1 - Role of adherens junctions and apical-basal polarity of neural stem/progenitor cells in the pathogenesis of neurodevelopmental disorders
T2 - a novel perspective on congenital Zika syndrome
AU - Bustamante, Felipe A.
AU - Miró, MarÍa Paz
AU - VelÁsquez, Zahady D.
AU - Molina, Luis
AU - Ehrenfeld, Pamela
AU - Rivera, Francisco J.
AU - Bátiz, Luis Federico
N1 - 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.
PY - 2019/8
Y1 - 2019/8
N2 - 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.
AB - 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.
KW - Adherens Junctions
KW - Animals
KW - Cell Polarity
KW - Humans
KW - Neural Stem Cells
KW - Neurodevelopmental Disorders
KW - Syndrome
KW - Zika Virus Infection
UR - http://www.scopus.com/inward/record.url?scp=85064172242&partnerID=8YFLogxK
U2 - 10.1016/j.trsl.2019.02.014
DO - 10.1016/j.trsl.2019.02.014
M3 - Review article
C2 - 30904442
AN - SCOPUS:85064172242
SN - 1931-5244
VL - 210
SP - 57
EP - 79
JO - Translational Research
JF - Translational Research
ER -