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Cells
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Hedgehog Signaling in Myelin Diseases and Inflammatory Disorders of the...
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Hedgehog Signaling in Myelin Diseases and Inflammatory Disorders of the Nervous System

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cells of the Nervous System".

Deadline for manuscript submissions: closed (31 May 2022) | Viewed by 13245

Special Issue Editor

Dr. Elisabeth Traiffort

E-Mail Website
Guest Editor
Diseases and Hormones of the Nervous System U1195 INSERM, Paris Saclay University, 80 Rue du Général Leclerc, 94276 Le Kremlin-Bicêtre, France
Interests: oligodendrocytes; microglia; astrocytes; myelin disorders; neural stem cells; Hedgehog signaling; androgens
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Until the end of the 20th century, proteins belonging to the Hedgehog family were essentially considered as morphogens acting at a distance from cells synthesizing them via the establishment of a concentration gradient and controling cell identities in the developing spinal cord. However, in recent decades, Hedgehog signaling has been found to be endowed with a multitude of other roles.

The involvement of Hedgehog signaling in the generation of oligodendrocytes, its requirement for proper development of peripheral nerve sheaths, as well as its implication in the maintenance of the blood–brain and blood–nerve barriers have raised the possibility that targeting Hedgehog signaling may open therapeutic perspectives towards demyelinating and inflammatory nervous system disorders.

The present Special Issue should provide an overview of the state-of-the art, namely, regarding the mechanisms underlying involvement of Hedgehog signaling in myelin production, the therapeutic potential of Hedgehog signaling modulators in the process of myelin maintenance or regeneration, the contribution of Hedgehog signals to design cell therapies for myelin diseases, Hedgehog-mediated control of the blood–brain and blood–nerve barriers, and the role of Hedgehog signaling in glial cells participating in neuroinflammation.

Dr. Elisabeth Traiffort
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • Hedgehog signaling
  • myelination
  • myelin repair
  • neuroinflammation
  • glial cells
  • blood¬brain barrier
  • blood–nerve barrier
  • hedgehog modulators
  • cell therapy
  • nerve injury

Related Special Issue

Published Papers (4 papers)

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12 pages, 1220 KiB  
Review
Hedgehog Signaling in CNS Remyelination
by Minxi Fang, Tao Tang, Mengsheng Qiu and Xiaofeng Xu
Cells 2022, 11(14), 2260; https://doi.org/10.3390/cells11142260 - 21 Jul 2022
Cited by 3 | Viewed by 2262
Abstract
Remyelination is a fundamental repair process in the central nervous system (CNS) that is triggered by demyelinating events. In demyelinating diseases, oligodendrocytes (OLs) are targeted, leading to myelin loss, axonal damage, and severe functional impairment. While spontaneous remyelination often fails in the progression [...] Read more.
Remyelination is a fundamental repair process in the central nervous system (CNS) that is triggered by demyelinating events. In demyelinating diseases, oligodendrocytes (OLs) are targeted, leading to myelin loss, axonal damage, and severe functional impairment. While spontaneous remyelination often fails in the progression of demyelinating diseases, increased understanding of the mechanisms and identification of targets that regulate myelin regeneration becomes crucial. To date, several signaling pathways have been implicated in the remyelination process, including the Hedgehog (Hh) signaling pathway. This review summarizes the current data concerning the complicated roles of the Hh signaling pathway in the context of remyelination. We will highlight the open issues that have to be clarified prior to bringing molecules targeting the Hh signaling to demyelinating therapy. Full article
(This article belongs to the Special Issue Hedgehog Signaling in Myelin Diseases and Inflammatory Disorders of the Nervous System)
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12 pages, 2530 KiB  
Review
New Tricks for an Old (Hedge)Hog: Sonic Hedgehog Regulation of Astrocyte Function
by A. Denise R. Garcia
Cells 2021, 10(6), 1353; https://doi.org/10.3390/cells10061353 - 30 May 2021
Cited by 7 | Viewed by 3279
Abstract
The Sonic hedgehog (Shh) molecular signaling pathway is well established as a key regulator of neurodevelopment. It regulates diverse cellular behaviors, and its functions vary with respect to cell type, region, and developmental stage, reflecting the incredible pleiotropy of this molecular signaling pathway. [...] Read more.
The Sonic hedgehog (Shh) molecular signaling pathway is well established as a key regulator of neurodevelopment. It regulates diverse cellular behaviors, and its functions vary with respect to cell type, region, and developmental stage, reflecting the incredible pleiotropy of this molecular signaling pathway. Although it is best understood for its roles in development, Shh signaling persists into adulthood and is emerging as an important regulator of astrocyte function. Astrocytes play central roles in a broad array of nervous system functions, including synapse formation and function as well as coordination and orchestration of CNS inflammatory responses in pathological states. Neurons are the source of Shh in the adult, suggesting that Shh signaling mediates neuron–astrocyte communication, a novel role for this multifaceted pathway. Multiple roles for Shh signaling in astrocytes are increasingly being identified, including regulation of astrocyte identity, modulation of synaptic organization, and limitation of inflammation. This review discusses these novel roles for Shh signaling in regulating diverse astrocyte functions in the healthy brain and in pathology. Full article
(This article belongs to the Special Issue Hedgehog Signaling in Myelin Diseases and Inflammatory Disorders of the Nervous System)
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11 pages, 724 KiB  
Review
Understanding the Heterogeneity of Human Pericyte Subsets in Blood–Brain Barrier Homeostasis and Neurological Diseases
by Diana G. Bohannon, Danielle Long and Woong-Ki Kim
Cells 2021, 10(4), 890; https://doi.org/10.3390/cells10040890 - 14 Apr 2021
Cited by 17 | Viewed by 4305
Abstract
Pericytes are increasingly recognized as being important in the control of blood–brain barrier permeability and vascular flow. Research on this important cell type has been hindered by widespread confusion regarding the phenotypic identity and nomenclature of pericytes and other perivascular cell types. In [...] Read more.
Pericytes are increasingly recognized as being important in the control of blood–brain barrier permeability and vascular flow. Research on this important cell type has been hindered by widespread confusion regarding the phenotypic identity and nomenclature of pericytes and other perivascular cell types. In addition, pericyte heterogeneity and mouse–human species differences have contributed to confusion. Herein we summarize our present knowledge on the identification of pericytes and pericyte subsets in humans, primarily focusing on recent findings in humans and nonhuman primates. Precise identification and definition of pericytes and pericyte subsets in humans may help us to better understand pericyte biology and develop new therapeutic approaches specifically targeting disease-associated pericyte subsets. Full article
(This article belongs to the Special Issue Hedgehog Signaling in Myelin Diseases and Inflammatory Disorders of the Nervous System)
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Other

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13 pages, 2483 KiB  
Brief Report
GLI3 Is Required for OLIG2+ Progeny Production in Adult Dorsal Neural Stem Cells
by Rebecca J. Embalabala, Asa A. Brockman, Amanda R. Jurewicz, Jennifer A. Kong, Kaitlyn Ryan, Cristina D. Guinto, Arturo Álvarez-Buylla, Chin Chiang and Rebecca A. Ihrie
Cells 2022, 11(2), 218; https://doi.org/10.3390/cells11020218 - 10 Jan 2022
Cited by 4 | Viewed by 2772
Abstract
The ventricular–subventricular zone (V-SVZ) is a postnatal germinal niche. It holds a large population of neural stem cells (NSCs) that generate neurons and oligodendrocytes for the olfactory bulb and (primarily) the corpus callosum, respectively. These NSCs are heterogeneous and generate different types of [...] Read more.
The ventricular–subventricular zone (V-SVZ) is a postnatal germinal niche. It holds a large population of neural stem cells (NSCs) that generate neurons and oligodendrocytes for the olfactory bulb and (primarily) the corpus callosum, respectively. These NSCs are heterogeneous and generate different types of neurons depending on their location. Positional identity among NSCs is thought to be controlled in part by intrinsic pathways. However, extrinsic cell signaling through the secreted ligand Sonic hedgehog (Shh) is essential for neurogenesis in both the dorsal and ventral V-SVZ. Here we used a genetic approach to investigate the role of the transcription factors GLI2 and GLI3 in the proliferation and cell fate of dorsal and ventral V-SVZ NSCs. We find that while GLI3 is expressed in stem cell cultures from both dorsal and ventral V-SVZ, the repressor form of GLI3 is more abundant in dorsal V-SVZ. Despite this high dorsal expression and the requirement for other Shh pathway members, GLI3 loss affects the generation of ventrally-, but not dorsally-derived olfactory interneurons in vivo and does not affect trilineage differentiation in vitro. However, loss of GLI3 in the adult dorsal V-SVZ in vivo results in decreased numbers of OLIG2-expressing progeny, indicating a role in gliogenesis. Full article
(This article belongs to the Special Issue Hedgehog Signaling in Myelin Diseases and Inflammatory Disorders of the Nervous System)
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