Hedgehog Signaling in Myelin Diseases and Inflammatory Disorders of the Nervous System—Second Edition

A special issue of Cells (ISSN 2073-4409).

Deadline for manuscript submissions: closed (31 October 2024) | Viewed by 1619

Special Issue Editor


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 the cells that synthesized them via the establishment of a concentration gradient and controlling 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 the 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

Benefits of Publishing in a Special Issue

  • Ease of navigation: Grouping papers by topic helps scholars navigate broad scope journals more efficiently.
  • Greater discoverability: Special Issues support the reach and impact of scientific research. Articles in Special Issues are more discoverable and cited more frequently.
  • Expansion of research network: Special Issues facilitate connections among authors, fostering scientific collaborations.
  • External promotion: Articles in Special Issues are often promoted through the journal's social media, increasing their visibility.
  • e-Book format: Special Issues with more than 10 articles can be published as dedicated e-books, ensuring wide and rapid dissemination.

Further information on MDPI's Special Issue policies can be found here.

Related Special Issue

Published Papers (1 paper)

Order results
Result details
Select all
Export citation of selected articles as:

Research

24 pages, 9065 KiB  
Article
Sonic Hedgehog Is an Early Oligodendrocyte Marker During Remyelination
by Mariagiovanna Russo, Amina Zahaf, Abdelmoumen Kassoussi, Ariane Sharif, Hélène Faure, Elisabeth Traiffort and Martial Ruat
Cells 2024, 13(21), 1808; https://doi.org/10.3390/cells13211808 - 1 Nov 2024
Cited by 1 | Viewed by 1351
Abstract
Failure of myelin regeneration by oligodendrocytes contributes to progressive decline in many neurological diseases. Here, using in vitro and in vivo rodent models, functional blockade, and mouse brain demyelination, we demonstrate that Sonic hedgehog (Shh) expression in a subset of oligodendrocyte progenitor cells [...] Read more.
Failure of myelin regeneration by oligodendrocytes contributes to progressive decline in many neurological diseases. Here, using in vitro and in vivo rodent models, functional blockade, and mouse brain demyelination, we demonstrate that Sonic hedgehog (Shh) expression in a subset of oligodendrocyte progenitor cells precedes the expression of myelin basic protein (MBP), a major myelin sheath protein. Primary cultures of rodent cortical oligodendrocytes show that Shh mRNA and protein are upregulated during oligodendrocyte maturation before the upregulation of MBP expression. Importantly, almost all MBP-positive cells are Shh positive during differentiation. During remyelination, we identify a rapid induction of Shh mRNA and peptide in oligodendroglial cells present in the demyelinated corpus callosum of mice, including a population of PDGFRα-expressing cells. Shh invalidation by an adeno-associated virus strategy demonstrates that the downregulation of Shh impairs the differentiation of oligodendrocytes in vitro and decreases MBP and myelin proteolipid protein expression in the demyelinated mouse brain at late stages of remyelination. We also report a parallel expression of Shh and MBP in oligodendroglial cells during early post-natal myelination of the mouse brain. Thus, we identify a crucial Shh signal involved in oligodendroglial cell differentiation and remyelination, with potential interest in the design of better-targeted remyelinating therapeutic strategies. Full article
Show Figures

Graphical abstract

Back to TopTop