scholarly journals Progesterone through Progesterone Receptor B Isoform Promotes Rodent Embryonic Oligodendrogenesis

Cells ◽  
2020 ◽  
Vol 9 (4) ◽  
pp. 960
Author(s):  
Juan Carlos González-Orozco ◽  
Aylin Del Moral-Morales ◽  
Ignacio Camacho-Arroyo
Keyword(s):  
Spinal Cord ◽  
Progesterone Receptor ◽  
Primary Cultures ◽  
Perinatal Period ◽  
Postnatal Life ◽  
Embryonic Mouse ◽  
Cord Injury ◽  
Proliferation And Differentiation ◽  
The Central Nervous System ◽  
Progesterone Receptor B

Oligodendrocytes are the myelinating cells of the central nervous system (CNS). These cells arise during the embryonic development by the specification of the neural stem cells to oligodendroglial progenitor cells (OPC); newly formed OPC proliferate, migrate, differentiate, and mature to myelinating oligodendrocytes in the perinatal period. It is known that progesterone promotes the proliferation and differentiation of OPC in early postnatal life through the activation of the intracellular progesterone receptor (PR). Progesterone supports nerve myelination after spinal cord injury in adults. However, the role of progesterone in embryonic OPC differentiation as well as the specific PR isoform involved in progesterone actions in these cells is unknown. By using primary cultures obtained from the embryonic mouse spinal cord, we showed that embryonic OPC expresses both PR-A and PR-B isoforms. We found that progesterone increases the proliferation, differentiation, and myelination potential of embryonic OPC through its PR by upregulating the expression of oligodendroglial genes such as neuron/glia antigen 2 (NG2), sex determining region Y-box9 (SOX9), myelin basic protein (MBP), 2′,3′-cyclic-nucleotide 3′-phosphodiesterase (CNP1), and NK6 homeobox 1 (NKX 6.1). These effects are likely mediated by PR-B, as they are blocked by the silencing of this isoform. The results suggest that progesterone contributes to the process of oligodendrogenesis during prenatal life through specific activation of PR-B.

PROTECTIVE EFFECT OF SOME SALTS 2-AMINOETHANESULFONIC ACID IN AN EXPERIMENTAL MODEL OF DEGENERATIVE SPINAL CORD INJURY

2020 ◽  
pp. 41-47
Author(s):  
Semeleva E.V. ◽  
Blinova E.V. ◽  
Zaborovsky A.V. ◽  
Vasilkina O.V. ◽  
Shukurov A.S.
Keyword(s):  
Spinal Cord ◽  
Morphological Changes ◽  
Male Rats ◽  
Zinc Salt ◽  
Control Group ◽  
Morphological Studies ◽  
Cord Injury ◽  
The Central Nervous System ◽  
Acid Compound ◽  
Lateral Sclerosis

In this work, we studied the pharmacological activity of zinc and magnesium salts of 2-aminoethanesulfonic acid in white non-linear male rats with amyotrophic lateral sclerosis, which was modeled by neurotoxicantsimplication into the pelvic part of spinal cord. After the reproduction of the pathology in animals, the indices of motor activity were recorded in the Rotarod test, and morphological studies of spinal cord sections stained according to Nisl in the Belshovsky modification were carried out. It was shown that the magnesium salt of 2-aminoethanesulfonic acid (compound LHT-317) to a greater extent reduces the development of motor disorders in experimental animals compared with the control group on the 4th day of observation. The course of intravenous administration of the studied compounds of 2-aminoethanesulfonic acid did not inhibit morphological changes in the spinal cord that develop in degenerative-dystrophic pathology of the central nervous system: connections. Moreover, if, against the background of treatment with zinc salt, the total area of motor zones in animals of the experimental group exceeded that of control rats, then the number of motoneurons did not differ from the control.

scholarly journals Planet of the AAVs: The Spinal Cord Injury Episode

Biomedicines ◽  
2021 ◽  
Vol 9 (6) ◽  
pp. 613
Author(s):  
Katerina Stepankova ◽  
Pavla Jendelova ◽  
Lucia Machova Urdzikova
Keyword(s):  
Spinal Cord ◽  
Gene Therapy ◽  
Spinal Cord Injury ◽  
Cell Types ◽  
Specific Cell ◽  
Adeno Associated Virus ◽  
Adequate Treatment ◽  
Cord Injury ◽  
The Central Nervous System ◽  
Transgene Delivery

The spinal cord injury (SCI) is a medical and life-disrupting condition with devastating consequences for the physical, social, and professional welfare of patients, and there is no adequate treatment for it. At the same time, gene therapy has been studied as a promising approach for the treatment of neurological and neurodegenerative disorders by delivering remedial genes to the central nervous system (CNS), of which the spinal cord is a part. For gene therapy, multiple vectors have been introduced, including integrating lentiviral vectors and non-integrating adeno-associated virus (AAV) vectors. AAV vectors are a promising system for transgene delivery into the CNS due to their safety profile as well as long-term gene expression. Gene therapy mediated by AAV vectors shows potential for treating SCI by delivering certain genetic information to specific cell types. This review has focused on a potential treatment of SCI by gene therapy using AAV vectors.

scholarly journals Biomaterial Approaches to Modulate Reactive Astroglial Response

2018 ◽  
Vol 205 (5-6) ◽  
pp. 372-395 ◽  
Author(s):  
Jonathan M. Zuidema ◽  
Ryan J. Gilbert ◽  
Manoj K. Gottipati
Keyword(s):  
Spinal Cord ◽  
Glial Scar ◽  
Secondary Injury ◽  
Injury Site ◽  
Beneficial Effects ◽  
Cord Injury ◽  
The Central Nervous System ◽  
Preclinical Animal Models

Over several decades, biomaterial scientists have developed materials to spur axonal regeneration and limit secondary injury and tested these materials within preclinical animal models. Rarely, though, are astrocytes examined comprehensively when biomaterials are placed into the injury site. Astrocytes support neuronal function in the central nervous system. Following an injury, astrocytes undergo reactive gliosis and create a glial scar. The astrocytic glial scar forms a dense barrier which restricts the extension of regenerating axons through the injury site. However, there are several beneficial effects of the glial scar, including helping to reform the blood-brain barrier, limiting the extent of secondary injury, and supporting the health of regenerating axons near the injury site. This review provides a brief introduction to the role of astrocytes in the spinal cord, discusses astrocyte phenotypic changes that occur following injury, and highlights studies that explored astrocyte changes in response to biomaterials tested within in vitro or in vivo environments. Overall, we suggest that in order to improve biomaterial designs for spinal cord injury applications, investigators should more thoroughly consider the astrocyte response to such designs.

scholarly journals Growth-Promoting Treatment Screening for Corticospinal Neurons in Mouse and Man

2020 ◽  
Vol 40 (8) ◽  
pp. 1327-1338
Author(s):  
Nicholas Hanuscheck ◽  
Andrea Schnatz ◽  
Carine Thalman ◽  
Steffen Lerch ◽  
Yvonne Gärtner ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Nervous System ◽  
Interleukin 4 ◽  
Regenerative Capacity ◽  
Beneficial Effects ◽  
Cord Injury ◽  
Tissue Culture Model ◽  
The Central Nervous System ◽  
Cone Formation ◽  
New Treatments

Abstract Neurons of the central nervous system (CNS) that project long axons into the spinal cord have a poor axon regenerative capacity compared to neurons of the peripheral nervous system. The corticospinal tract (CST) is particularly notorious for its poor regeneration. Because of this, traumatic spinal cord injury (SCI) is a devastating condition that remains as yet uncured. Based on our recent observations that direct neuronal interleukin-4 (IL-4) signaling leads to repair of axonal swellings and beneficial effects in neuroinflammation, we hypothesized that IL-4 acts directly on the CST. Here, we developed a tissue culture model for CST regeneration and found that IL-4 promoted new growth cone formation after axon transection. Most importantly, IL-4 directly increased the regenerative capacity of both murine and human CST axons, which corroborates its regenerative effects in CNS damage. Overall, these findings serve as proof-of-concept that our CST regeneration model is suitable for fast screening of new treatments for SCI.

scholarly journals Acellularized spinal cord scaffolds incorporating bpV(pic)/PLGA microspheres promote axonal regeneration and functional recovery after spinal cord injury

RSC Advances ◽  
2020 ◽  
Vol 10 (32) ◽  
pp. 18677-18686
Author(s):  
Jia Liu ◽  
Kai Li ◽  
Ke Huang ◽  
Chengliang Yang ◽  
Zhipeng Huang ◽  
...  
Keyword(s):  
Spinal Cord ◽  
Central Nervous System ◽  
Spinal Cord Injury ◽  
Nervous System ◽  
Axonal Regeneration ◽  
Traumatic Injury ◽  
High Rate ◽  
Plga Microspheres ◽  
Cord Injury ◽  
The Central Nervous System

Spinal cord injury (SCI) is a traumatic injury to the central nervous system (CNS) with a high rate of disability and a low capability of self-recovery.

scholarly journals Extrinsic and Intrinsic Regulation of Axon Regeneration by MicroRNAs after Spinal Cord Injury

2016 ◽  
Vol 2016 ◽  
pp. 1-11 ◽  
Author(s):  
Ping Li ◽  
Zhao-Qian Teng ◽  
Chang-Mei Liu
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Axonal Regeneration ◽  
Axon Regeneration ◽  
Therapeutic Potential ◽  
Glial Scar ◽  
Scar Formation ◽  
Extrinsic Factors ◽  
Cord Injury ◽  
The Central Nervous System

Spinal cord injury is a devastating disease which disrupts the connections between the brain and spinal cord, often resulting in the loss of sensory and motor function below the lesion site. Most injured neurons fail to regenerate in the central nervous system after injury. Multiple intrinsic and extrinsic factors contribute to the general failure of axonal regeneration after injury. MicroRNAs can modulate multiple genes’ expression and are tightly controlled during nerve development or the injury process. Evidence has demonstrated that microRNAs and their signaling pathways play important roles in mediating axon regeneration and glial scar formation after spinal cord injury. This article reviews the role and mechanism of differentially expressed microRNAs in regulating axon regeneration and glial scar formation after spinal cord injury, as well as their therapeutic potential for promoting axonal regeneration and repair of the injured spinal cord.

scholarly journals Neuroplasticity After Spinal Cord Injury and Training: An Emerging Paradigm Shift in Rehabilitation and Walking Recovery

2006 ◽  
Vol 86 (10) ◽  
pp. 1406-1425 ◽  
Author(s):  
Andrea L Behrman ◽  
Mark G Bowden ◽  
Preeti M Nair
Keyword(s):  
Spinal Cord ◽  
Spinal Cord Injury ◽  
Nervous System ◽  
Paradigm Shift ◽  
Clinical Findings ◽  
Cord Injury ◽  
Rehabilitation Concepts ◽  
The Central Nervous System ◽  
Walking Recovery ◽  
Physiologically Based Approach

AbstractPhysical rehabilitation after spinal cord injury has been based on the premise that the nervous system is hard-wired and irreparable. Upon this assumption, clinicians have compensated for irremediable sensorimotor deficits using braces, assistive devices, and wheelchairs to achieve upright and seated mobility. Evidence from basic science, however, demonstrates that the central nervous system after injury is malleable and can learn, and this evidence has challenged our current assumptions. The evidence is especially compelling concerning locomotion. The purpose of this perspective article is to summarize the evidence supporting an impending paradigm shift from compensation for deficits to rehabilitation as an agent for walking recovery. A physiologically based approach for the rehabilitation of walking has developed, translating evidence for activity-dependent neuroplasticity after spinal cord injury and the neurobiological control of walking. Advanced by partnerships among neuroscientists, clinicians, and researchers, critical rehabilitation concepts are emerging for activity-based therapy to improve walking recovery, with promising clinical findings.

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