A Distal to Proximal Gradient of Human Choroid Plexus Development, with Antagonistic Expression of Glut1 and AQP1 in Mature Cells vs. Calbindin and PCNA in Proliferative Cells

Castañeyra-Ruiz, Leandro; González-Marrero, Ibrahim; Hernández-Abad, Luis G.; Carmona-Calero, Emilia M.; Meyer, Gundela; Castañeyra-Perdomo, Agustín

doi:10.3389/fnana.2016.00087

Cited by 15 publications

(7 citation statements)

References 22 publications

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“…The choroid plexus is active in secretion of the cerebrospinal fluid (CSF) and in barrier functions early in corticogenesis (Castañeyra‐Ruiz et al. ). The secretion of signalling molecules from the ChP into the CSF can regulate the behaviour of neural stem cells, which are in direct contact with the CSF.…”

Section: Discussionmentioning

confidence: 99%

Cajal‐Retzius neurons are required for the development of the human hippocampal fissure

et al. 2019

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Cajal-Retzius neurons (CRN) are the main source of Reelin in the marginal zone of the developing neocortex and hippocampus (HC). They also express the transcription factor p73 and are complemented by laterappearing GABAergic Reelin + interneurons. The human dorsal HC forms at gestational week 10 (GW10), when it develops a rudimentary Ammonic plate and incipient dentate migration, although the dorsal hippocampal fissure (HF) remains shallow and contains few CRN. The dorsal HC transforms into the indusium griseum (IG), concurrently with the rostro-caudal appearance of the corpus callosum, by GW14-17. Dorsal and ventral HC merge at the site of the former caudal hem, which is located at the level of the future atrium of the lateral ventricle and closely connected with the choroid plexus. The ventral HC forms at GW11 in the temporal lobe. The ventral HF is wide open at GW14-16 and densely populated by large numbers of CRNs. These are in intimate contact with the meninges and meningeal blood vessels, suggesting signalling through diverse pathways. At GW17, the fissure deepens and begins to fuse, although it is still marked by p73/Reelin + CRNs. The p73KO mouse illustrates the importance of p73 in CRN for HF formation. In the mutant, Tbr1/Reelin + CRNs are born in the hem but do not leave it and subsequently disappear, so that the mutant cortex and HC lack CRN from the onset of corticogenesis. The HF is absent, which leads to profound architectonic alterations of the HC. To determine which p73 isoform is important for HF formation, isoform-specific TAp73-and DeltaNp73deficient embryonic and early postnatal mice were examined. In both mutants, the number of CRNs was reduced, but each of their phenotypes was much milder than in the global p73KO mutant missing both isoforms. In the TAp73KO mice, the HF of the dorsal HC failed to form, but was present in the ventral HC. In the DeltaNp73KO mice, the HC had a mild patterning defect along with a shorter HF. Complex interactions between both isoforms in CRNs may contribute to their crucial activity in the developing brain.Sections were deparaffinized, hydrated, and boiled in 10 mM citrate buffer (pH 6) for 20 min for antigen retrieval, rinsed in Trisbuffered saline (TBS, pH 7.6, 0.05 M), and incubated in the primary antibodies overnight in a humid chamber. After rinsing, they were incubated in the corresponding biotinylated secondary antibodies (rabbit anti-mouse IgG or goat anti-rabbit IgG; Dako, Glostrup, Denmark), diluted at 1 : 200 in TBS, followed by incubation with avidin-biotin complex (ABC, DAKO) in TBS. Bound peroxidase was

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Section: Discussionmentioning

confidence: 99%

Cajal‐Retzius neurons are required for the development of the human hippocampal fissure

et al. 2019

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“…In addition, GRC and neural progenitor cell loss due to VZ disruption are associated with abnormalities in neurogenesis such as abnormal neuroblast migration as intrinsic mechanisms of congenital [ 57 , 58 , 59 ] and posthemorrhagic hydrocephalus [ 60 , 61 ]. AQPs have been highly studied in brain development under control [ 24 , 28 , 62 ] and hydrocephalic conditions [ 63 , 64 , 65 , 66 , 67 , 68 , 69 , 70 , 71 ]. It has been proposed that the AQP variations are associated with hydrocephalus-compensatory mechanisms to decrease the production and increase the absorption of CSF [ 66 , 67 , 68 , 69 , 70 , 71 ].…”

Section: Introductionmentioning

confidence: 99%

AQP4, Astrogenesis, and Hydrocephalus: A New Neurological Perspective

Castañeyra-Ruiz

González-Marrero

Hernández-Abad

et al. 2022

IJMS

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Aquaporin 4 (AQP4) is a cerebral glial marker that labels ependymal cells and astrocytes’ endfeet and is the main water channel responsible for the parenchymal fluid balance. However, in brain development, AQP4 is a marker of glial stem cells and plays a crucial role in the pathophysiology of pediatric hydrocephalus. Gliogenesis characterization has been hampered by a lack of biomarkers for precursor and intermediate stages and a deeper understanding of hydrocephalus etiology is needed. This manuscript is a focused review of the current research landscape on AQP4 as a possible biomarker for gliogenesis and its influence in pediatric hydrocephalus, emphasizing reactive astrogliosis. The goal is to understand brain development under hydrocephalic and normal physiologic conditions.

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“…In the Lmx1aCre:: β-catenin LOF telencephalon, the CP appears dysmorphic and disorganized (Figure 2). From E14.5, some regions of the CP lose their characteristic ribbon-like appearance and fail to express the transcription factor Otx2 , which is required for CP specification (Johansson et al 2013), or Aquaporin 1 ( Aqp1 ), a channel critical for CSF production (Kim and Jung 2012; Castañeyra-Ruiz et al 2016). Though TTR expression appears relatively unaffected, the expression of E-CADHERIN is perturbed, consistent with the abnormally folded appearance of the CP.…”

Section: Resultsmentioning

confidence: 99%

Constitutive activation of canonical Wnt signaling disrupts choroid plexus epithelial fate

Parichha

Suresh

Chatterjee

et al. 2020

Preprint

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The choroid plexus (CP) secretes cerebrospinal fluid and is critical for the development and function of the brain. In the telencephalon, the CP epithelium (CPe) arises from the Wnt- and Bmp- expressing cortical hem. We examined the role of canonical Wnt signaling in CPe development and report that the mouse and human embryonic CPe expresses molecules in this pathway. Either loss of function or constitutive activation of β-catenin, a key mediator of canonical Wnt signaling, causes a profound disruption of mouse CPe development. Loss of β-catenin results in a dysmorphic CPe, while constitutive activation of β-catenin causes a loss of CPe identity and a transformation of this tissue to a hippocampal-like identity. Aspects of this phenomenon are recapitulated in human embryonic stem cell (hESC)-derived organoids. Our results indicate that canonical Wnt signaling is required in a precisely regulated manner for normal CP development in the mammalian brain.

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A Distal to Proximal Gradient of Human Choroid Plexus Development, with Antagonistic Expression of Glut1 and AQP1 in Mature Cells vs. Calbindin and PCNA in Proliferative Cells

Cited by 15 publications

References 22 publications

Cajal‐Retzius neurons are required for the development of the human hippocampal fissure

Cajal‐Retzius neurons are required for the development of the human hippocampal fissure

AQP4, Astrogenesis, and Hydrocephalus: A New Neurological Perspective

Constitutive activation of canonical Wnt signaling disrupts choroid plexus epithelial fate

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