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Article ; Online: Filamin A and Big2: a shared endocytic pathway.

Sheen, Volney L

Bioarchitecture

2014 Volume 4, Issue 2, Page(s) 53–57

Abstract: Neural proliferation, migration and differentiation require reorganization of the actin cytoskeleton and regulation of vesicle trafficking to provide stability in maintaining cell adhesions, allow for changes in cell shape, and establishing cell polarity. ...

Abstract	Neural proliferation, migration and differentiation require reorganization of the actin cytoskeleton and regulation of vesicle trafficking to provide stability in maintaining cell adhesions, allow for changes in cell shape, and establishing cell polarity. Human disorders involving the actin-binding Filamin A (FLNA) and vesicle trafficking Brefeldin-associated guanine exchange factor 2 (BIG2 is encoded by the ARFGEF2 gene) proteins are implicated in these various developmental processes, resulting in a malformation of cortical development called periventricular heterotopia (nodules along the ventricular lining) and microcephaly (small brain). Here we discuss several recent reports from our laboratory that demonstrate a shared role for both proteins in actin-associated vesicle trafficking, which is required to maintain the expression and stability of cell adhesion and cell cycle associated molecules during cortical development. While changes in FLNA and BIG2 have first been linked to disorders involving the central nervous system, increasing reports suggest they are associated with aberrant development of various other organ systems in the body. These studies suggest that vesicle trafficking defects in FLN-GEF dependent pathways may contribute to a much broader phenotype than previously realized.
Language	English
Publishing date	2014-04-07
Publishing country	United States
Document type	Journal Article
ISSN	1949-100X
ISSN (online)	1949-100X
DOI	10.4161/bioa.28516
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article: Filamin A mediated Big2 dependent endocytosis: From apical abscission to periventricular heterotopia.

Sheen, Volney L

Tissue barriers

2014 Volume 2, Page(s) e29431

Abstract: Periventricular heterotopia (PH) is one of the most common malformations of cortical development (MCD). Nodules along the lateral ventricles of the brain, disruption of the ventricular lining, and a reduced brain size are hallmarks of this disorder. PH ... ...

Abstract	Periventricular heterotopia (PH) is one of the most common malformations of cortical development (MCD). Nodules along the lateral ventricles of the brain, disruption of the ventricular lining, and a reduced brain size are hallmarks of this disorder. PH results in a disruption of the neuroependyma, inhibition of neural proliferation and differentiation, and altered neuronal migration. Human mutations in the genes encoding the actin-binding Filamin A (FLNA) and the vesicle trafficking Brefeldin A-associated guanine exchange factor 2 (BIG2 is encoded by the ARFGEF2 gene) proteins are implicated in PH formation. Recent studies have shown that the transition from proliferating neural progenitors to post-mitotic neurons relies on apical abscission along the neuroepithelium. This mechanism involves an actin dependent contraction of the apical portion of a neural progenitor along the ventricular lining to complete abscission. Actin also maintains stability of various cell adhesion molecules along the neuroependyma. Loss of cadherin directs disassembly of the primary cilium, which transduces sonic-hedgehog (Shh) signaling. Shh signaling is required for continued proliferation. In this context, apical abscission regulates neuronal progenitor exit and migration from the ventricular zone by detachment from the neuroependyma, relies on adhesion molecules that maintain the integrity of the neuroepithelial lining, and directs neural proliferation. Each of these processes is disrupted in PH, suggesting that genes causal for this MCD, may fundamentally mediate apical abscission in cortical development. Here we discuss several recent reports that demonstrate a coordinated role for actin and vesicle trafficking in modulating neural development along the neurepithelium, and potentially the neural stem cell to neuronal transition.
Language	English
Publishing date	2014-06-16
Publishing country	United States
Document type	Journal Article
ISSN	2168-8362
ISSN	2168-8362
DOI	10.4161/tisb.29431
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Article ; Online: Seizure or syncope: lessons over time.

Sheen, Volney L

Journal of clinical neuroscience : official journal of the Neurosurgical Society of Australasia

2012 Volume 19, Issue 3, Page(s) 481–483

Abstract: A 25-year-old woman with recurrent syncopal episodes presented with a first time generalized tonic clonic (GTC) seizure. She had experienced two prior fainting spells lasting seconds and associated with diet pills and dehydration. She had another similar ...

Abstract	A 25-year-old woman with recurrent syncopal episodes presented with a first time generalized tonic clonic (GTC) seizure. She had experienced two prior fainting spells lasting seconds and associated with diet pills and dehydration. She had another similar spell prior to falling, sustaining a laceration to the right posterior occiput, and having a witnessed GTC seizure. Her scalp electroencephalography (EEG) showed left temporal slowing with sharp features. T1-weighted and T2-weighted MRI revealed two moderately enhancing focal lesions within the left frontal and temporal regions. These findings raised the possibility of an underlying seizure focus. Repeat imaging studies of this patient 1 month later, however, demonstrated resolution of these findings and an area of encephalomalacia, consistent with a traumatic coup contrecoup injury. A repeat EEG was normal. Therefore, the cause of the loss of consciousness was due to syncope with the consequent head injury giving rise to an isolated seizure. Understanding the underlying cause of a seizure is important in dictating treatment. In this setting the patient was not initiated on seizure medication and has done well.
MeSH term(s)	Adult ; Brain/pathology ; Craniocerebral Trauma/etiology ; Electroencephalography ; Encephalomalacia/etiology ; Epilepsy, Tonic-Clonic/complications ; Female ; Humans ; Image Processing, Computer-Assisted ; Magnetic Resonance Imaging ; Seizures/complications ; Seizures/etiology ; Syncope/complications ; Tomography, X-Ray Computed
Language	English
Publishing date	2012-01-14
Publishing country	Scotland
Document type	Case Reports ; Journal Article ; Research Support, N.I.H., Extramural
ZDB-ID	1193674-5
ISSN	1532-2653 ; 0967-5868
ISSN (online)	1532-2653
ISSN	0967-5868
DOI	10.1016/j.jocn.2011.06.017
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Article: Periventricular Heterotopia: Shuttling of Proteins through Vesicles and Actin in Cortical Development and Disease.

Sheen, Volney L

Scientifica

2012 Volume 2012, Page(s) 480129

Abstract: During cortical development, proliferating neural progenitors exhibit polarized apical and basolateral membranes that are maintained by tightly controlled and membrane-specific vesicular trafficking pathways. Disruption of polarity through impaired ... ...

Abstract	During cortical development, proliferating neural progenitors exhibit polarized apical and basolateral membranes that are maintained by tightly controlled and membrane-specific vesicular trafficking pathways. Disruption of polarity through impaired delivery of proteins can alter cell fate decisions and consequent expansion of the progenitor pool, as well as impact the integrity of the neuroependymal lining. Loss of neuroependymal integrity disrupts radial glial scaffolding and alters initial neuronal migration from the ventricular zone. Vesicle trafficking is also required for maintenance of lipid and protein cycling within the leading and trailing edge of migratory neurons, as well as dendrites and synapses of mature neurons. Defects in this transport machinery disrupt neuronal identity, migration, and connectivity and give rise to a malformation of cortical development termed as periventricular heterotopia (PH). PH is characterized by a reduction in brain size, ectopic clusters of neurons localized along the lateral ventricle, and epilepsy and dyslexia. These anatomical anomalies correlate with developmental impairments in neural progenitor proliferation and specification, migration from loss of neuroependymal integrity and neuronal motility, and aberrant neuronal process extension. Genes causal for PH regulate vesicle-mediated endocytosis along an actin cytoskeletal network. This paper explores the role of these dynamic processes in cortical development and disease.
Language	English
Publishing date	2012-10-22
Publishing country	Egypt
Document type	Journal Article ; Review
ZDB-ID	2672321-9
ISSN	2090-908X
ISSN	2090-908X
DOI	10.6064/2012/480129
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Article: Cytoskeletal proteins in cortical development and disease: actin associated proteins in periventricular heterotopia.

Lian, Gewei / Sheen, Volney L

Frontiers in cellular neuroscience

2015 Volume 9, Page(s) 99

Abstract: The actin cytoskeleton regulates many important cellular processes in the brain, including cell division and proliferation, migration, and cytokinesis and differentiation. These developmental processes can be regulated through actin dependent vesicle and ...

Abstract	The actin cytoskeleton regulates many important cellular processes in the brain, including cell division and proliferation, migration, and cytokinesis and differentiation. These developmental processes can be regulated through actin dependent vesicle and organelle movement, cell signaling, and the establishment and maintenance of cell junctions and cell shape. Many of these processes are mediated by extensive and intimate interactions of actin with cellular membranes and proteins. Disruption in the actin cytoskeleton in the brain gives rise to periventricular heterotopia (PH), a malformation of cortical development, characterized by abnormal neurons clustered deep in the brain along the lateral ventricles. This disorder can give rise to seizures, dyslexia and psychiatric disturbances. Anatomically, PH is characterized by a smaller brain (impaired proliferation), heterotopia (impaired initial migration) and disruption along the neuroependymal lining (impaired cell-cell adhesion). Genes causal for PH have also been implicated in actin-dependent processes. The current review provides mechanistic insight into actin cytoskeletal regulation of cortical development in the context of this malformation of cortical development.
Language	English
Publishing date	2015-04-01
Publishing country	Switzerland
Document type	Journal Article ; Review
ZDB-ID	2452963-1
ISSN	1662-5102
ISSN	1662-5102
DOI	10.3389/fncel.2015.00099
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Article: Hyperostosis cranii ex vacuo from ventricular shunting

Sheen, Volney L.

Journal of Pediatric Neurology

2011 Volume 09, Issue 04, Page(s) 509–511

Language	English
Publishing date	2011-12-01
Publisher	Georg Thieme Verlag KG
Publishing place	Stuttgart ; New York
Document type	Article
ISSN	1875-9041 ; 1304-2580
ISSN (online)	1875-9041
ISSN	1304-2580
DOI	10.3233/JPN-2011-0511
Database	Thieme publisher's database

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Article ; Online: Periventricular Heterotopia

Volney L. Sheen

Scientifica, Vol

Shuttling of Proteins through Vesicles and Actin in Cortical Development and Disease

2012 Volume 2012

Abstract	During cortical development, proliferating neural progenitors exhibit polarized apical and basolateral membranes that are maintained by tightly controlled and membrane-specific vesicular trafficking pathways. Disruption of polarity through impaired delivery of proteins can alter cell fate decisions and consequent expansion of the progenitor pool, as well as impact the integrity of the neuroependymal lining. Loss of neuroependymal integrity disrupts radial glial scaffolding and alters initial neuronal migration from the ventricular zone. Vesicle trafficking is also required for maintenance of lipid and protein cycling within the leading and trailing edge of migratory neurons, as well as dendrites and synapses of mature neurons. Defects in this transport machinery disrupt neuronal identity, migration, and connectivity and give rise to a malformation of cortical development termed as periventricular heterotopia (PH). PH is characterized by a reduction in brain size, ectopic clusters of neurons localized along the lateral ventricle, and epilepsy and dyslexia. These anatomical anomalies correlate with developmental impairments in neural progenitor proliferation and specification, migration from loss of neuroependymal integrity and neuronal motility, and aberrant neuronal process extension. Genes causal for PH regulate vesicle-mediated endocytosis along an actin cytoskeletal network. This paper explores the role of these dynamic processes in cortical development and disease.
Keywords	Medicine ; R ; Science ; Q
Subject code	571
Language	English
Publishing date	2012-01-01T00:00:00Z
Publisher	Hindawi Limited
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: DNMT3L promotes neural differentiation by enhancing STAT1 and STAT3 phosphorylation independent of DNA methylation.

Qin, Lin / Qiao, Chong / Sheen, Volney / Wang, Yu / Lu, Jie

Progress in neurobiology

2021 Volume 201, Page(s) 102028

Abstract: Previously, we reported global hypermethylation in DS might be attributed to the overexpression of HSA21 gene DNMT3L, which can enhance DNMT3A and DNMT3B activities in DNA methylation. To test this hypothesis, we compared the DNA methylation and RNA ... ...

Abstract	Previously, we reported global hypermethylation in DS might be attributed to the overexpression of HSA21 gene DNMT3L, which can enhance DNMT3A and DNMT3B activities in DNA methylation. To test this hypothesis, we compared the DNA methylation and RNA expression profiles of early-differentiated human neuroprogenitors with and without DNMT3L overexpression. We found DNMT3L overexpression only moderately increased the DNA methylation of limited genes, yet significantly altered global RNA expression of genes involved in neural differentiation. We further found that DNMT3L bound STAT1 or STAT3, and increased its phosphorylation and nuclear translocation, which in turn activated the expression of transcription factors including HES3, ASCL1, NEUROD2 and NEUROG2 and CDK inhibitor CDKN1A, which promoted cell cycle exit and neural differentiation. This phenomenon was also confirmed in Dnmt3l conditional knockin mice, which could be rescued by STAT1 and STAT3 phosphorylation inhibitors (Fludarabine and SH-4-54) but not DNA methylation inhibitor (Decitabine). These results suggest that DNMT3L play an important role during neurodevelopment independent of DNA methylation, which may contribute to the abnormal phenotypes observed in Down syndrome cortex.
MeSH term(s)	Animals ; Basic Helix-Loop-Helix Transcription Factors ; Cell Differentiation ; DNA (Cytosine-5-)-Methyltransferases/genetics ; DNA Methylation ; Mice ; Nerve Tissue Proteins ; Phosphorylation ; RNA ; STAT1 Transcription Factor
Chemical Substances	Basic Helix-Loop-Helix Transcription Factors ; Nerve Tissue Proteins ; Neurog2 protein, mouse ; STAT1 Transcription Factor ; Stat1 protein, mouse ; RNA (63231-63-0) ; Dnmt3l protein, mouse (EC 2.1.1.-) ; DNA (Cytosine-5-)-Methyltransferases (EC 2.1.1.37)
Language	English
Publishing date	2021-02-23
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	185535-9
ISSN	1873-5118 ; 0301-0082
ISSN (online)	1873-5118
ISSN	0301-0082
DOI	10.1016/j.pneurobio.2021.102028
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Article ; Online: Promoting nerve cell functions on hydrogels grafted with poly(L-lysine).

Cai, Lei / Lu, Jie / Sheen, Volney / Wang, Shanfeng

Biomacromolecules

2012 Volume 13, Issue 2, Page(s) 342–349

Abstract: We present a novel photopolymerizable poly(L-lysine) (PLL) and use it to modify polyethylene glycol ...

Abstract	We present a novel photopolymerizable poly(L-lysine) (PLL) and use it to modify polyethylene glycol diacrylate (PEGDA) hydrogels for creating a better, permissive nerve cell niche. Compared with their neutral counterparts, these PLL-grafted hydrogels greatly enhance pheochromocytoma (PC12) cell survival in encapsulation, proliferation, and neurite growth and also promote neural progenitor cell proliferation and differentiation capacity, represented by percentages of both differentiated neurons and astrocytes. The role of efficiently controlled substrate stiffness in regulating nerve cell behavior is also investigated and a polymerizable cationic small molecule, [2-(methacryloyloxy)ethyl]-trimethylammonium chloride (MTAC), is used to compare with this newly developed PLL. The results indicate that these PLL-grafted hydrogels are promising biomaterials for nerve repair and regeneration.
MeSH term(s)	Animals ; Astrocytes/cytology ; Astrocytes/drug effects ; Astrocytes/physiology ; Biocompatible Materials/chemical synthesis ; Biocompatible Materials/pharmacology ; Cell Adhesion/drug effects ; Cell Differentiation/drug effects ; Cell Proliferation/drug effects ; Cell Survival/drug effects ; Humans ; Hydrogels ; Light ; Magnetic Resonance Spectroscopy ; Neurons/cytology ; Neurons/drug effects ; Neurons/physiology ; PC12 Cells ; Photochemical Processes ; Polyethylene Glycols/chemistry ; Polylysine/chemical synthesis ; Polylysine/pharmacology ; Polymerization ; Rats ; Tissue Scaffolds
Chemical Substances	Biocompatible Materials ; Hydrogels ; poly(ethylene glycol)diacrylate ; Polylysine (25104-18-1) ; Polyethylene Glycols (3WJQ0SDW1A)
Language	English
Publishing date	2012-02-01
Publishing country	United States
Document type	Journal Article ; Research Support, U.S. Gov't, Non-P.H.S.
ISSN	1526-4602
ISSN (online)	1526-4602
DOI	10.1021/bm201763n
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Optimal poly(L-lysine) grafting density in hydrogels for promoting neural progenitor cell functions.

Cai, Lei / Lu, Jie / Sheen, Volney / Wang, Shanfeng

Biomacromolecules

2012 Volume 13, Issue 5, Page(s) 1663–1674

Abstract: Recently, we have developed a photopolymerizable poly(L-lysine) (PLL) that can be covalently ...

Abstract	Recently, we have developed a photopolymerizable poly(L-lysine) (PLL) that can be covalently incorporated into poly(ethylene glycol) diacrylate (PEGDA) hydrogels to improve their bioactivity by providing positive charges. To explore the potential of these PLL-grafted PEGDA hydrogels as a cell delivery vehicle and luminal filler in nerve guidance conduits for peripheral and central nerve regeneration, we varied the number of pendent PLL chains in the hydrogels by photo-cross-linking PEGDA with weight compositions of PLL (φ(PLL)) of 0, 1, 2, 3, and 5%. We further investigated the effect of PLL grafting density on E14 mouse neural progenitor cell (NPC) behavior including cell viability, attachment, proliferation, differentiation, and gene expression. The amount of actually grafted PLL and charge densities were characterized, showing a proportional increase with the feed composition φ(PLL). NPC viability in 3D hydrogels was significantly improved in a PLL grafting density-dependent manner at days 7 and 14 postencapsulation. Similarly, NPC attachment and proliferation were promoted on the PLL-grafted hydrogels with increasing φ(PLL) up to 2%. More intriguingly, NPC lineage commitment was dramatically altered by the amount of grafted PLL chains in the hydrogels. NPC differentiation demonstrated a parabolic or nonmonotonic dependence on φ(PLL), resulting in cells mostly differentiated toward mature neurons with extensive neurite formation and astrocytes rather than oligodendrocytes on the PLL-grafted hydrogels with φ(PLL) of 2%, whereas the neutral hydrogels and PLL-grafted hydrogels with higher φ(PLL) of 5% support NPC differentiation less. Gene expression of lineage markers further illustrated this trend, indicating that PLL-grafted hydrogels with an optimal φ(PLL) of 2% could be a promising cell carrier that promoted NPC functions for treatment of nerve injuries.
MeSH term(s)	Animals ; Cell Differentiation/drug effects ; Cell Proliferation/drug effects ; Cell Survival/drug effects ; Hydrogels/chemistry ; Hydrogels/pharmacology ; Mice ; Models, Molecular ; Molecular Structure ; Neural Stem Cells/cytology ; Neural Stem Cells/drug effects ; Neural Stem Cells/metabolism ; Polyethylene Glycols/chemistry ; Polylysine/chemistry ; Polylysine/pharmacology ; Structure-Activity Relationship
Chemical Substances	Hydrogels ; Polylysine (25104-18-1) ; Polyethylene Glycols (3WJQ0SDW1A)
Language	English
Publishing date	2012-05-03
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Research Support, U.S. Gov't, Non-P.H.S.
ISSN	1526-4602
ISSN (online)	1526-4602
DOI	10.1021/bm300381d
Database	MEDical Literature Analysis and Retrieval System OnLINE

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