The Effects of Inflammation on Glial Fibrillary Acidic Protein Expression in Satellite Cells of the Dorsal Root Ganglion

Siemionow, Krzysztof; Klimczak, Aleksandra; Brzezicki, Grzegorz; Siemionow, Maria; McLain, Robert F.

doi:10.1097/brs.0b013e3181ab1f68

Cited by 34 publications

(24 citation statements)

References 32 publications

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“…These data are in accordance with several recent studies proposing that, after peripheral injury and/or inflammation, SGCs undergo relevant reactive biochemical and phenotypic changes (such as activation, proliferation and hypertrophy) that might be related to the establishment/maintenance of certain pathological and painful states [6], [9], [11], [26]–[28]. In fact, GFAP expression was found to be increased in inflamed DRGs, at 7 days of model induction (chromic gut suture application onto the DRG) [6], as well as in the trigeminal ganglia of rats with orofacial inflammatory pain [27].…”

Section: Discussionsupporting

confidence: 93%

“…In fact, GFAP expression was found to be increased in inflamed DRGs, at 7 days of model induction (chromic gut suture application onto the DRG) [6], as well as in the trigeminal ganglia of rats with orofacial inflammatory pain [27]. Additionally, two days post-CFA injection into the whisker pad area, the mean percentage of trigeminal ganglia neurons encircled by GFAP and IL-1beta-immunoreactive cells was significantly increased compared with controls [25].…”

Section: Discussionmentioning

confidence: 94%

“…However, following nerve injury, inflammation or viral infection, GFAP becomes detectable in the SGCs that become activated by the pathological insult. Thus, in the PNS, GFAP expression is commonly used as a marker of SGCs activation [4]–[6]. Although SGCs' properties and functions have not yet been fully studied, it is now clear that these cells take an important part in the “intercellular communication” [3] with the neuronal cells they are in contact with.…”

Section: Introductionmentioning

confidence: 99%

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Satellite Glial Cells Surrounding Primary Afferent Neurons Are Activated and Proliferate during Monoarthritis in Rats: Is There a Role for ATF3?

2014

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Joint inflammatory diseases are debilitating and very painful conditions that still lack effective treatments. Recently, glial cells were shown to be crucial for the development and maintenance of chronic pain, constituting novel targets for therapeutic approaches. At the periphery, the satellite glial cells (SGCs) that surround the cell bodies of primary afferents neurons in the dorsal root ganglia (DRG) display hypertrophy, proliferation, and activation following injury and/or inflammation. It has been suggested that the expression of neuronal injury factors might initially trigger these SGCs-related events. We then aimed at evaluating if SGCs are involved in the establishment/maintenance of articular inflammatory pain, by using the monoarthritis (MA) model, and if the neuronal injury marker activating transcriptional factor 3 (ATF3) is associated with these SGCs' reactive changes. Western Blot (WB) analysis of the glial fibrillary acidic protein (GFAP) expression was performed in L4-L5 DRGs from control non-inflamed rats and MA animals at different time-points of disease (4, 7, and 14d, induced by complete Freund's adjuvant injection into the left hind paw ankle joint). Data indicate that SGCs activation is occurring in MA animals, particularly after day 7 of disease evolution. Additionally, double-immunostaining for ATF3 and GFAP in L5 DRG sections shows that SGCs's activation significantly increases around stressed neurons at 7d of disease, when compared with control animals. The specific labelling of GFAP in SGCs rather than in other cell types was also confirmed by immunohistochemical labeling. Finally, BrdU incorporation indicates that proliferation of SGCs is also significantly increased after 7 days of MA. Data indicate that SGCs play an important role in the mechanisms of articular inflammation, with 7 days of disease being a critical time-point in the MA model, and suggest that ATF3 might be involved in SGCs' reactive changes such as activation.

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Section: Discussionsupporting

confidence: 93%

Section: Discussionmentioning

confidence: 94%

Section: Introductionmentioning

confidence: 99%

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Satellite Glial Cells Surrounding Primary Afferent Neurons Are Activated and Proliferate during Monoarthritis in Rats: Is There a Role for ATF3?

2014

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“…Several studies correlate glial activation with an increase in the expression of different proteins, including GFAP (23,24). A neutralizing antibody against the FKN receptor (AbCX3CR1; 10 μg per DRG) was administered into the DRG (L5).…”

Section: Discussionmentioning

confidence: 99%

Fractalkine mediates inflammatory pain through activation of satellite glial cells

Souza

Talbot

Lotufo

et al. 2013

Proc. Natl. Acad. Sci. U.S.A.

129

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The activation of the satellite glial cells (SGCs) surrounding the dorsal root ganglion (DRG) neurons appears to play a role in pathological pain. We tested the hypothesis that fractalkine, which is constitutively expressed by primary nociceptive neurons, is the link between peripheral inflammation and the activation of SGCs and is thus responsible for the genesis of the inflammatory pain. The injection of carrageenin into the rat hind paw induced a decrease in the mechanical nociceptive threshold (hypernociception), which was associated with an increase in mRNA and GFAP protein expression in the DRG. Both events were inhibited by antifractalkine antibody administered directly into the DRG (L5) [intraganglionar (i.gl.)]. The administration of fractalkine into the DRG (L5) produced mechanical hypernociception in a dose-, time-, and CX3C receptor-1 (CX3CR1)-dependent manner. Fractalkine's hypernociceptive effect appears to be indirect, as it was reduced by local treatment with anti-TNF-α antibody, IL-1-receptor antagonist, or indomethacin. Accordingly, the in vitro incubation of isolated and cultured SGC with fractalkine induced the production/ release of TNF-α, IL-1β, and prostaglandin E 2 . Finally, treatment with i.gl. fluorocitrate blocked fractalkine (i.gl.)-and carrageenin (paw)-induced hypernociception. Overall, these results suggest that, during peripheral inflammation, fractalkine is released in the DRG and contributes to the genesis of inflammatory hypernociception. Fractalkine's effect appears to be dependent on the activation of the SGCs, leading to the production of TNFα, IL-1β, and prostanoids, which are likely responsible for the maintenance of inflammatory pain. Thus, these results indicate that the inhibition of fractalkine/ CX3CR1 signaling in SGCs may serve as a target to control inflammatory pain.cytokines | hyperalgesia | primary sensitization | nociception

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“…Gsr Key cellular antioxidant enzyme (Franco et al, 2007); upregulated by oxidative stress in the hippocampus (Torres, 2012) Manganese superoxide dismutase Sod2 Enzyme that reduces damage by superoxide (H. F. Huang, Guo, Cao, Shi, & Xia, 2012) and upregulated by oxidative stress in hippocampus (Furuta et al, 1995; RodriguezMartinez, Martinez, Espinosa-Garcia, Maldonado, & Rivas-Arancibia, 2013) Heme oxygenase-1 Hmox1 Enzyme strongly upregulated by oxidative stress in brain (Guerra et al, 2013) Apoptosis/inflammation Bcl-2-associated X protein Bax Proapoptotic member of Bcl-2 family (Engel, Plesnila, Prehn, & Henshall, 2011); key role in regulating intrinsic apoptotic signaling (Cheng, Gulbins, & Siemen, 2011) Bcl-2-associated agonist of cell death Bad Positively regulates cell apoptosis (Dave et al, 2011;Siemionow, Klimczak, Brzezicki, Siemionow, & McLain, 2009) Glial fibrillary acidic protein Gfap Marker of CNS inflammation (gliosis; Giovannoni, 2006;Siemionow et al, 2009) Protection from injury Tumor necrosis factor Tnf Regulates survival of injured hippocampal neurons (Bernardino et al, 2005;Viviani, Corsini, Galli, & Marinovich, 1998;Yang, Lindholm, Konishi, Li, & Shen, 2002) …”

Section: Glutathione Reductasementioning

confidence: 97%

Effects of Intraventricular Methotrexate on Neuronal Injury and Gene Expression in a Rat Model

Moore

Merkle

Byrne

et al. 2016

Biological Research For Nursing

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Central nervous system (CNS)-directed treatment for acute lymphoblastic leukemia, used to prevent disease recurrence in the brain, is essential for survival. Systemic and intrathecal methotrexate, commonly used for CNS-directed treatment, have been associated with cognitive problems during and after treatment. The cortex, hippocampus, and caudate putamen, important brain regions for learning and memory, may be involved in methotrexate-induced brain injury. Objectives of this study were to (1) quantify neuronal degeneration in selected regions of the cortex, hippocampus, and caudate putamen and (2) measure changes in the expression of genes with known roles in oxidant defense, apoptosis/inflammation, and protection from injury. Male Sprague Dawley rats were administered 2 or 4 mg/kg of methotrexate diluted in artificial cerebrospinal fluid (aCSF) or aCSF only into the left cerebral lateral ventricle. Gene expression changes were measured using customized reverse transcription (RT)(2) polymerase chain reaction arrays. The greatest percentage of degenerating neurons in methotrexate-treated animals was in the medial region of the cortex; percentage of degenerating neurons in the dentate gyrus and cornu ammonis 3 regions of the hippocampus was also greater in rats treated with methotrexate compared to perfusion and vehicle controls. There was a greater percentage of degenerating neurons in the inferior cortex of control versus methotrexate-treated animals. Eight genes involved in protection from injury, oxidant defense, and apoptosis/inflammation were significantly downregulated in different brain regions of methotrexate-treated rats. To our knowledge, this is the first study to investigate methotrexate-induced injury in selected brain regions and gene expression changes using a rat model of intraventricular drug administration.

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The Effects of Inflammation on Glial Fibrillary Acidic Protein Expression in Satellite Cells of the Dorsal Root Ganglion

Cited by 34 publications

References 32 publications

Satellite Glial Cells Surrounding Primary Afferent Neurons Are Activated and Proliferate during Monoarthritis in Rats: Is There a Role for ATF3?

Satellite Glial Cells Surrounding Primary Afferent Neurons Are Activated and Proliferate during Monoarthritis in Rats: Is There a Role for ATF3?

Fractalkine mediates inflammatory pain through activation of satellite glial cells

Effects of Intraventricular Methotrexate on Neuronal Injury and Gene Expression in a Rat Model

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