Glial cell-specific mechanisms of TGF-β1 induction by IL-1 in cerebral cortex

Cunha, Anna da; Jefferson, Jane A.; Jackson, Robert W.; Vitkoviç, Ljubiša

doi:10.1016/0165-5728(93)90214-j

Cited by 138 publications

(89 citation statements)

References 48 publications

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“…The upregulation is not confined to the regions of neuropathology. For example, IL-1 is elevated in cortex of individuals who died with AIDS 15 although the frequency of HIV-1-infected cells in the cortex is lower than in other regions. 16 Evidence reviewed here indicates that both central and systemic perturbations induce or upregulate IL-1 and TNF␣ expression and this 'cytokine signal' propagates through the parenchyma sometimes to distant regions that are apparently unconnected by neu- 17 (By 'perturbations' we mean central or systemic stimuli that alter IL-1 and TNF␣ expression.)…”

Section: Introductionmentioning

confidence: 98%

Cytokine signals propagate through the brain

et al. 2000

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Interleukin-1 (IL-1) and tumor necrosis factor alpha (TNF␣) are proinflammatory cytokines that are constitutively expressed in healthy, adult brain where they mediate normal neural functions such as sleep. They are neuromodulators expressed by and acting on neurons and glia. IL-1 and TNF␣ expression is upregulated in several important diseases/disorders. Upregulation of IL-1 and/or TNF␣ expression, elicited centrally or systemically, propagates through brain parenchyma following specific spatio-temporal patterns. We propose that cytokine signals propagate along neuronal projections and extracellular diffusion pathways by molecular cascades that need to be further elucidated. This elucidation is a prerequisite for better understanding of reciprocal interactions between nervous, endocrine and immune systems. Molecular Psychiatry (2000) 5, 604-615.

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Section: Introductionmentioning

confidence: 98%

Cytokine signals propagate through the brain

et al. 2000

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“…An important physiologic role of TGF-b within the brain appears to be termination of the glial proliferative response to injury and/or cytokine-induced stimulation (Lindholm et al, 1992;da Cunha et al, 1993). Among quiescent newborn rat cerebral glia, serum induction of DNA synthesis is delayed and attenuated by TGF-b1.…”

Section: Role Of Tgf-b As a Negative Regulatory Cytokine In Glioblastomamentioning

confidence: 99%

TGF-β, Neuronal Stem Cells and Glioblastoma

Golestaneh

Mishra

2005

Oncogene

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Transforming growth factor beta (TGF-b) signaling leads to a number of biological end points involving cell growth, differentiation, and morphogenesis. Typically, the cellular effect accompanies an induction of mesodermal cell fate and inhibition of neural cell differentiation. However, during pathological conditions, these defined effects of TGF-b can be reversed; for example, the growthinhibitory effect is replaced with its tumor promoting ability. A multitude of factors and cross-signaling pathways have been reported to be involved in modulating the dual effects of TGF-b. In this review, we focus on the potential role of TGF-b signal transduction during development of neural progenitor cells and its relation to glioblastoma development from neural stem cells.

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“…This review emphasizes TGF-p1, because its activities during responses to brain injury are better understood than those of TGF-p2 and 433. For most information cited without references, see general reviews and recent papers Roberts and Sporn, 1990;da Cunha et al, 1993;Morgan et al, 1993;Pasinetti et al, 19931. bridization [da Cunha et al, 1993;Nichols and Finch, 1991;Unsicker et al, 19911. At a cellular level, the meninges and choroid plexus of normal rodent and human brains clearly contain both TGF-p1 mRNA and protein.…”

Section: Introductionmentioning

confidence: 99%

“…TGF-p1 mRNA could also be present in neurons, but at lower prevalence. There is also considerable TGF-p1 mRNA in primary cultures of microglia, astrocytes, and oligodendroglia [e.g., Lindholm et al, 1990;da Cunha et al, 1993;Morganti-Kossmann et al, 19921. This broad range of brain cell types is consistent with the widespread expression of the TGF-p genes in non-neural tissues, depending on the circumstances.…”

Section: Introductionmentioning

confidence: 99%

TGF‐β1 is an organizer of responses to neurodgeneration

Finch

Laping

Morgan

et al. 1993

J of Cellular Biochemistry

191

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TGF-PI mRNA and protein were recently found to increase in animal brains after experimental lesions that cause local deafferentation or neuron death. Elevations of TGF-PI mRNA after lesions are prominent in microglia but are also observed in neurons and astrocytes. Moreover, TGF-PI mRNA autoinduces its own mRNA in the brain. These responses provide models for studying the increases of TGF-PI protein observed in PAiamyloid-containing extracellular plaques of Alzheimer's disease (AD) and Down's syndrome (DS) and in brain cells of AIDS victims.Involvement of TGF-01 in these human brain disorders is discussed in relation to the potent effects of TGF-PI on wound healing and inflammatory responses in peripheral tissues.We hypothesize that TGF-PI and possibly other TGF-P peptides have organizing roles in responses to neurodegeneration and brain injury that are similar to those observed in non-neural tissues. Work from many laboratories has shown that activities of TGF-P peptides on brain cells include chemotaxis, modification of extracellular matrix, and regulation of cytoskeletal gene expression and of neurotrophins. Similar activities of the TGF-P's are well established in other tissues.

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Glial cell-specific mechanisms of TGF-β1 induction by IL-1 in cerebral cortex

Cited by 138 publications

References 48 publications

Cytokine signals propagate through the brain

Cytokine signals propagate through the brain

TGF-β, Neuronal Stem Cells and Glioblastoma

TGF‐β1 is an organizer of responses to neurodgeneration

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