Enhanced expression of a protein antigen (JI‐31 antigen, 30 kilodaltons) by reactive astrocytes in lacerated spinal cord

Predy, R.; Malhotra, S. K.; Das, Gopal D.

doi:10.1002/jnr.490190403

Cited by 18 publications

(9 citation statements)

References 22 publications

(11 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Several years ago, Malhotra and colleagues developed a monoclonal antibody (Mab J1-31), which labels reactive astrocytes located close to a surgical lesion site (Malhotra et al 1984;Singh et al 1986;Predy et al 1988;Malhotra et al 1993). The present labeling patterns obtained with Mab 6.17 appear therefore very similar to that obtained by Malhotra and colleagues with the Mab J1-31.…”

Section: Discussionsupporting

confidence: 88%

“…The present labeling patterns obtained with Mab 6.17 appear therefore very similar to that obtained by Malhotra and colleagues with the Mab J1-31. However, after a lacerated-type surgical lesion of the spinal cord, it has been shown that Mab J1-31 recognizes reactive astrocytes in the immediate vicinity of the lesion, whereas reactive astrocytes located at some distance were not immunostained (Predy et al 1988;Malhotra et al 1993). In contrast, Mab 6.17 labels reactive astrocytes that are both close and at a distance from a surgical lesion.…”

Section: Discussionmentioning

confidence: 85%

See 1 more Smart Citation

Immunocytochemical characterization of a new marker of fibrous and reactive astrocytes

Ridet

Alonso

Chauvet

et al. 1995

Cell and Tissue Research

View full text Add to dashboard Cite

A specific monoclonal antiserum (Mab 6.17) inducing a strong immunostaining of the neuromuscular junction has been used to detect the possible occurrence of the corresponding antigen throughout the intact or lesioned central nervous system of adult rats. In intact animals, 6.17-immunolabeling was essentially detected in astrocyte-like structures located in white matter fasciculi of the brain, such as the optic tract, corpus callosum, fornix, and in the white matter of the spinal cord. The astroglial nature of such 6.17-immunolabeled profiles was verified by performing double or triple immunofluorescent labeling with Mab 6.17 and with specific antisera against astrocytic markers, such as S100 protein, glial fibrillary acidic protein and vimentin. In the white matter, all the structures reactive to Mab 6.17 were also reactive to antibodies against S100 protein, glial fibrillary acidic protein and vimentin. On the other hand, astrocytes of the grey matter that were immunoreactive to S100 and glial fibrillary acidic protein but negative to vimentin, were devoid of 6.17-immunoreactivity. After lesions including stab wound through the diencephalon or transection of the spinal cord, a marked increase of 6.17-immunostaining was noted in the regions surrounding the lesions. In these regions, 6.17-immunolabeling was associated with S100-, GFAP- and vimentin-positive astrocytes constituting the glial scar. The ultrastructural localization of 6.17-immunoreactivity indicated that, similar to glial fibrillary acidic protein and vimentin, the recognized antigen was mainly associated with gliofilaments. These observations indicate that, in the central nervous system of adult rats, Mab 6.17 recognizes a molecule associated with gliofilaments, which is essentially associated to reactive astrocytes expressing high levels of vimentin.

show abstract

Section: Discussionsupporting

confidence: 88%

Section: Discussionmentioning

confidence: 85%

Immunocytochemical characterization of a new marker of fibrous and reactive astrocytes

Ridet

Alonso

Chauvet

et al. 1995

Cell and Tissue Research

View full text Add to dashboard Cite

show abstract

“…The use of an astrocyte/low-grade astrocytoma marker demonstrated that Oct4 is re-expressed in astrocytes during injury. In fact, this monoclonal antibody (Mab JI-31) recognizes an intracellular protein antigen expressed by astrocytes and upregulated in reactive astrocytes [30]. Consistent with our hypothesis, the Oct4-positive cells were costained with the J1-31 anti-astrocyte antibody in the area of the lesion (Fig.…”

Section: Resultssupporting

confidence: 80%

Inflammation Promotes a Conversion of Astrocytes into Neural Progenitor Cells via NF-κB Activation

et al. 2015

View full text Add to dashboard Cite

Brain inflammation, a common feature in neurodegenerative diseases, is a complex series of events, which can be detrimental and even lead to neuronal death. Nonetheless, several studies suggest that inflammatory signals are also positively influencing neural cell proliferation, survival, migration, and differentiation. Recently, correlative studies suggested that astrocytes are able to dedifferentiate upon injury and may thereby re-acquire neural stem cell (NSC) potential. However, the mechanism underlying this dedifferentiation process upon injury remains unclear. Here, we report that during the early response of reactive gliosis, inflammation induces a conversion of mature astrocytes into neural progenitors. A TNF treatment induces the decrease of specific astrocyte markers, such as glial fibrillary acidic protein (GFAP) or genes related to glycogen metabolism, while a subset of these cells re-expresses immaturity markers, such as CD44, Musashi-1, and Oct4. Thus, TNF treatment results in the appearance of cells that exhibit a neural progenitor phenotype and are able to proliferate and differentiate into neurons and/or astrocytes. This dedifferentiation process is maintained as long as TNF is present in the culture medium. In addition, we highlight a role for Oct4 in this process, since the TNF-induced dedifferentiation can be prevented by inhibiting Oct4 expression. Our results show that activation of the NF-κB pathway through TNF plays an important role in the dedifferentiation of astrocytes via the re-expression of Oct4. These findings indicate that the first step of reactive gliosis is in fact a dedifferentiation process of resident astrocytes mediated by the NF-κB pathway.Electronic supplementary materialThe online version of this article (doi:10.1007/s12035-015-9428-3) contains supplementary material, which is available to authorized users.

show abstract

“…8A,B). Overall, the GFAP staining of the host cord resembled that seen after an injury to the adult rat spinal cord (Houle and Reier, 1988;Predy et al, 1988).…”

Section: Immunohistochemical Analysis Of the Host Interaction With Thmentioning

confidence: 68%

Grafting of Encapsulated BDNF-Producing Fibroblasts into the Injured Spinal Cord Without Immune Suppression in Adult Rats

Tobias

Dhoot

Wheatley

et al. 2001

Journal of Neurotrauma

View full text Add to dashboard Cite

Grafting of genetically modified cells that express therapeutic products is a promising strategy in spinal cord repair. We have previously grafted BDNF-producing fibroblasts (FB/BDNF) into injured spinal cord of adult rats, but survival of these cells requires a strict protocol of immune suppression with cyclosporin A (CsA). To develop a transplantation strategy without the detrimental effects of CsA, we studied the properties of FB/BDNF that were encapsulated in alginate-poly-L-ornithine, which possesses a semipermeable membrane that allows production and diffusion of a therapeutic product while protecting the cells from the host immune system. Our results show that encapsulated FB/BDNF, placed in culture, can survive, secrete bioactive BDNF and continue to grow for at least one month. Furthermore, encapsulated cells that have been stored in liquid nitrogen retain the ability to grow and express the transgene. Encapsulated FB/BDNF survive for at least one month after grafting into an adult rat cervical spinal cord injury site in the absence of immune suppression. Transgene expression decreased within two weeks after grafting but resumed when the cells were harvested and re-cultured, suggesting that soluble factors originating from the host immune response may contribute to the downregulation. In the presence of capsules that contained FB/BDNF, but not cell-free control capsules, there were many axons and dendrites at the grafting site. We conclude that alginate encapsulation of genetically modified cells may be an effective strategy for delivery of therapeutic products to the injured spinal cord and may provide a permissive environment for host axon growth in the absence of immune suppression.

show abstract

Enhanced expression of a protein antigen (JI‐31 antigen, 30 kilodaltons) by reactive astrocytes in lacerated spinal cord

Cited by 18 publications

References 22 publications

Immunocytochemical characterization of a new marker of fibrous and reactive astrocytes

Immunocytochemical characterization of a new marker of fibrous and reactive astrocytes

Inflammation Promotes a Conversion of Astrocytes into Neural Progenitor Cells via NF-κB Activation

Grafting of Encapsulated BDNF-Producing Fibroblasts into the Injured Spinal Cord Without Immune Suppression in Adult Rats

Contact Info

Product

Resources

About