Regulation by Interleukin‐1 of Nerve Growth Factor Secretion and Nerve Growth Factor mRNA Expression in Rat Primary Astroglial Cultures

Carman-Krzan, M; Vigé, Xavier; Wise, Bradley C.

doi:10.1111/j.1471-4159.1991.tb08197.x

Cited by 145 publications

(56 citation statements)

References 43 publications

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“…IL-1␤ is widely recognized for its ability to regulate the expression of many different molecules involved in determining neuronal death (59). IL-1␤ may also induce the release of neurotropins (60), but it can also initiate the production of toxic reactive oxygen species, such as NO, through the induction of iNOS (61). Of interest, U373 cells exhibited greater reactivity than primary astrocytes in response to thrombin and TF, especially for IL-1␤, which probably reflected residual effects of thrombin in serum and the need to culture primary astrocytes in high levels of serum for survival before experimental use.…”

Section: Discussionmentioning

confidence: 99%

Up-Regulation of Proteinase-Activated Receptor 1 Expression in Astrocytes During HIV Encephalitis

Boven¹,

Vergnolle²,

Henry³

et al. 2003

The Journal of Immunology

113

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Proteinase-activated receptor 1 (PAR-1) is a G protein-coupled receptor that is activated by thrombin and is implicated in the pathogenesis of inflammation. Although PAR-1 is expressed on immunocompetent cells within the brain such as astrocytes, little is known about its role in the pathogenesis of inflammatory brain diseases. Herein, we investigated PAR-1 regulation of brain inflammation by stimulating human astrocytic cells with thrombin or the selective PAR-1-activating peptide. Activated cells expressed significantly increased levels of IL-1β, inducible NO synthase, and PAR-1 mRNA. Moreover, supernatants of these same cells were neurotoxic, which was inhibited by an N-methyl-d-aspartate receptor antagonist. Striatal implantation of the PAR-1-activating peptide significantly induced brain inflammation and neurobehavioral deficits in mice compared with mice implanted with the control peptide or saline. Since HIV-related neurological disease is predicated on brain inflammation and neuronal injury, the expression of PAR-1 in HIV encephalitis (HIVE) was investigated. Immunohistochemical analysis revealed that PAR-1 and (pro)-thrombin protein expression was low in control brains, but intense immunoreactivity was observed on astrocytes in HIVE brains. Similarly, PAR-1 and thrombin mRNA levels were significantly increased in HIVE brains compared with control and multiple sclerosis brains. These data indicated that activation and up-regulation of PAR-1 probably contribute to brain inflammation and neuronal damage during HIV-1 infection, thus providing new therapeutic targets for the treatment of HIV-related neurodegeneration.

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Section: Discussionmentioning

confidence: 99%

Up-Regulation of Proteinase-Activated Receptor 1 Expression in Astrocytes During HIV Encephalitis

Boven¹,

Vergnolle²,

Henry³

et al. 2003

The Journal of Immunology

113

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“…Cytokine activation of astrocytes also induces elevated levels of nerve growth factor (NGF) expression (6,7,8). NGF is a member of a family of neurotrophic factors, called neurotrophins, which includes brain-derived neurotrophic factor (BDNF), neurotrophin-3 (NT-3), and neurotrophin-4/5 (NT-4/ 5).…”

mentioning

confidence: 99%

Regulation of Nerve Growth Factor mRNA by Interleukin-1 in Rat Hippocampal Astrocytes Is Mediated by NFκB

Friedman

Thakur²,

Seidman³

et al. 1996

Journal of Biological Chemistry

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Cytokines such as interleukin-1␤ (Il-1) are produced in the brain during development and during inflammatory processes that result from lesions or disease. One function of Il-1 in the brain appears to be the stimulation of astrocytes to proliferate and produce a variety of cytokines and trophic factors, including nerve growth factor. The mechanisms by which Il-1 exerts its actions on astrocytes remain poorly defined. We present evidence that this cytokine elicits activation of the NFB transcription factor and that this transcription factor mediates effects of Il-1 on nerve growth factor mRNA expression. Elucidation of the processes by which cytokines activate astrocytes and influence trophic factor expression may provide insight into mechanisms governing inflammatory processes within the central nervous system.

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“…In contrast, its staining was strong and widely distributed around the arteries and in the PALS of SCID mice, suggesting that its production is usually inhibited by the immune system in normal animals. IL-1␤ is known to stimulate NGF production in fibroblasts, astrocytes, and other cell types (34,35), and we reported that it promoted sympathetic neurite outgrowth in lymphoid tissues by stimulating NGF production, using a rodent sympathetic ganglion and lymphoid tissue explant coculture system (11,12). Because IL-1␤ levels were found to be higher in SCID mice, it may have been responsible, at least in part, for the elevated levels of NGF in the spleen of these animals.…”

Section: Discussionmentioning

confidence: 99%

Neuritogenic Effects of T Cell-Derived IL-3 on Mouse Splenic Sympathetic Neurons In Vivo

Kannan-Hayashi

Okamura

Hattori

et al. 2008

The Journal of Immunology

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To determine the role played by lymphocytes and cytokines in the growth of sympathetic neurons in vivo, the innervation and cytokine levels were examined in the spleens of SCID mice that lack T and B cells. Splenic noradrenaline, nerve growth factor (NGF), and IL-1β levels were elevated in SCID mice. Immunohistochemical examination revealed that the density of tyrosine hydroxylase-positive (TH+) fibers of splenic central arteries in SCID mice was increased compared with wild-type C.B-17 mice, while SCID mice had significantly fewer TH+ fibers in their periarteriolar lymphatic sheaths (PALS). Two weeks after SCID mice were injected with C.B-17 splenic T cells, their TH+ fiber staining increased in the PALS. IL-3 levels increased significantly in SCID mice following T cell reconstitution, and the administration of anti-IL-3 Ab blocked the above T cell-induced increase in innervation in the PALS. Anti-IL-3 treatment also inhibited the regeneration of splenic sympathetic neurons in C.B-17 mice after they were chemically sympathetomized with 6-hydroxydopamine. Depletion of NK cells by anti-asialo GM1 promoted the splenic innervation in SCID mice, while there were no significant changes in the innervation between CD8+ T cell-deficient β2-microglobulin knockout mice and their wild type. Our results suggest that T cells (probably CD4+ Th cells but not CD8+ CTLs) play a role in regulating the sympathetic innervation of the spleen; this effect appeared to be mediated, at least in part, by IL-3. On the contrary, NK cells may exert an inhibitory effect on the sympathetic innervation.

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Regulation by Interleukin‐1 of Nerve Growth Factor Secretion and Nerve Growth Factor mRNA Expression in Rat Primary Astroglial Cultures

Cited by 145 publications

References 43 publications

Up-Regulation of Proteinase-Activated Receptor 1 Expression in Astrocytes During HIV Encephalitis

Up-Regulation of Proteinase-Activated Receptor 1 Expression in Astrocytes During HIV Encephalitis

Regulation of Nerve Growth Factor mRNA by Interleukin-1 in Rat Hippocampal Astrocytes Is Mediated by NFκB

Neuritogenic Effects of T Cell-Derived IL-3 on Mouse Splenic Sympathetic Neurons In Vivo

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