Interleukin-1 Stimulation of Astroglial Proliferation After Brain Injury

Giulian, Dana; Lachman, Lawrence B.

doi:10.1126/science.3872478

Cited by 829 publications

(323 citation statements)

References 19 publications

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“…It has been reported that astrocytes produce IL-1 [37] and IL-1 stimulates the proliferation of astrocytes [38]. Our results suggest that IL-1 induces the production of several cytokines and glucocorticoids regulate their production negatively in astrocytes.…”

Section: ~Bsupporting

confidence: 56%

Dexamethasone regulation of the expression of cytokine mRNAs induced by interleukin‐1 in the astrocytoma cell line U373MG

Nishida¹,

Nakai²,

Kawakami³

et al. 1989

FEBS Letters

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BSF-2/IL-6, GM-CSF and IL-lfl mRNAs were induced by recombinant IL-I in human astrocytoma cell line U373MG. The induction of BSF-2/IL-6 and IL-lfl mRNAs did not require de novo protein synthesis while that of GM-CSF mRNA required a newly synthesized protein. Dexamethasone inhibited the induction of these cytokine mRNAs by IL-I. This process seems to require continued protein synthesis. These results suggest that the production of these cytokines are positively and negatively controlled by IL-1 and glucocorticoids, respectively, in astrocytes.

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Section: ~Bsupporting

confidence: 56%

Dexamethasone regulation of the expression of cytokine mRNAs induced by interleukin‐1 in the astrocytoma cell line U373MG

Nishida¹,

Nakai²,

Kawakami³

et al. 1989

FEBS Letters

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“…Degeneration of severed axon tracts appears to lead to gliosis, even in regions remote from the site of trauma in the brain or spinal cord (Barrett et al, 1981;Fitch and Silver, 1997a;Massey, et al, 2006;Murray et al, 1990;Steward and Trimmer, 1997). Cytokines or other molecules that may trigger gliosis include TNF-alpha (Rostworowski et al, 1997), endothelin-1 (Hama et al, 1997), IL-1 (Giulian and Lachman, 1985), IL-6 (Chiang et al, 1994), thrombin (Nishino et al, 1993), and CNTF (Kahn et al, 1995). Some of these may originate as soluble serum factors, or they can be directly produced by astrocytes, activated microglia, or peripheral macrophages.…”

Section: Triggers For the Production Of Inhibitory Extracellular Matrixmentioning

confidence: 99%

CNS injury, glial scars, and inflammation: Inhibitory extracellular matrices and regeneration failure

Fitch

Silver

2008

Experimental Neurology

877

657

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Spinal cord and brain injuries lead to complex cellular and molecular interactions within the central nervous system in an attempt to repair the initial tissue damage. Many studies have illustrated the importance of the glial cell response to injury, and the influences of inflammation and wound healing processes on the overall morbidity and permanent disability that result. The abortive attempts of neuronal regeneration after spinal cord injury are influenced by inflammatory cell activation, reactive astrogliosis and the production of both growth promoting and inhibitory extracellular molecules. Despite the historical perspective that the glial scar was a mechanical barrier to regeneration, inhibitory molecules in the forming scar and methods to overcome them have suggested molecular modification strategies to allow neuronal growth and functional regeneration. Unlike myelin associated inhibitory molecules, which remain at largely static levels before and after central nervous system trauma, inhibitory extracellular matrix molecules are dramatically upregulated during the inflammatory stages after injury providing a window of opportunity for the delivery of candidate therapeutic interventions. While high dose methylprednisolone steroid therapy alone has not proved to be the solution to this difficult clinical problem, other strategies for modulating inflammation and changing the make up of inhibitory molecules in the extracellular matrix are providing robust evidence that rehabilitation after spinal cord and brain injury has the potential to significantly change the outcome for what was once thought to be permanent disability.

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“…A number of diverse stimuli have been shown to induce astrocyte hyperplasia or hypertrophy, in cluding cytokines (Fontana et aI., 1980;Merrill et aI., 1984;Guilian and Lachman, 1985), brain derived glial growth factors (Sheffield and Kim, 1977;Pruss et aI. , 1982;Lemke and Brockes, 1984;Guilian and Young, 1986), epidermal growth factors (Brunk et aI.…”

Section: Discussionmentioning

confidence: 99%

The Two Patterns of Reactive Astrocytosis in Postischemic Rat Brain

Petito

Morgello

Felix

et al. 1990

J Cereb Blood Flow Metab

320

140

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Summary:The distribution and time course of postisch emic astrocyte hypertrophy and hyperplasia and the re lationship to neuronal viability or necrosis was studied in rats subjected to 30 min of carotid and vertebral artery occlusion followed by reperfusion from 3 h to 5 weeks. Intermediate filaments (IFs) were evaluated by electron microscopy, IF proteins by immunohistochemistry, and astrocyte division by [ 3 H]thymidine uptake. Glial fibril lary acidic protein (GF AP) increased in damaged and nondamaged brain regions by 2 days and was associated with cell enlargement, increases in IF, and transformation of GF AP-negative into GF AP-positive glia. Cell hyper trophy and increased GFAP persisted only in regions of neuronal necrosis whereas the number and size of GF AP positive astrocytes returned to control levels in nondam aged regions by 2 weeks. Astrocyte hyperplasia was notInteractions between astrocytes and neurons have gained increasing importance since in vitro studies have shown that metabolic properties of as trocytes are important in maintaining the normal homeostasis of the interstitial fluid compartment of the brain. These cells have high-affinity uptake sys tems (Faivre-Bauman et aI., 1974; Hertz et aI., 1974;Hertz, 1978; Cooper et aI., 1979;Kimelberg et al., 1982;Kraig et al., 1986) for many of the extra cellular ions and excitatory neurotransmitters that are elevated after ischemia, including hydrogen ions and glutamate, both of which have been implicated in causing ischemic injury. Thus, the initiation of Received January 15, 1990; revised April 23, 1990; accepted April 25, 1990.Address correspondence and reprint requests to Dr. C. K. Petito at Department of Pathology, Cornell University Medical College, 1300 York Avenue, New York, NY 10021, U.S.A.Abbreviations used: ABC, avidin-biotin complex; GFAP, glial fibrillary acidic protein; HRP, horseradish peroxidase; IFs, in termediate filaments; OD, optical density; RER, rough endoplas mic reticulum. 850seen until 3 days and was confined to damaged brain re gions. Vimentin-positive astrocytes were numerous by 2 days in damaged brain and remained only in those regions at 5 weeks. The data demonstrate that reactive astrocy to sis develops in undamaged brain, but is reversible with prolonged survival, whereas reactive astrocytosis that ac companies structural brain damage persists for prolonged periods and is associated with hyperplasia, as well as hy pertrophy. In addition, the results show that astrocyte expression of vimentin is more specific than GFAP in identifying regions of permanent ischemic injury during the early postischemic period.

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Interleukin-1 Stimulation of Astroglial Proliferation After Brain Injury

Cited by 829 publications

References 19 publications

Dexamethasone regulation of the expression of cytokine mRNAs induced by interleukin‐1 in the astrocytoma cell line U373MG

Dexamethasone regulation of the expression of cytokine mRNAs induced by interleukin‐1 in the astrocytoma cell line U373MG

CNS injury, glial scars, and inflammation: Inhibitory extracellular matrices and regeneration failure

The Two Patterns of Reactive Astrocytosis in Postischemic Rat Brain

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