Tumor necrosis factor stimulates the synthesis and secretion of biologically active nerve growth factor in non-neuronal cells.

Hattori, Akira; Tanaka, Eiko; Murase, Kouhei; Ishida, Nobuhiro; Chatani, Yuji; Tsujimoto, Masafumi; Hayashi, Kyozo; Kohno, Michiaki

doi:10.1016/s0021-9258(18)53813-8

Cited by 145 publications

(8 citation statements)

References 35 publications

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“…Interestingly, we observed the induction of NGF-␤ in parallel with a small increase in TNF-␣. TNF-␣ induces NGF-␤ in fibroblasts (77) and may regulate levels of NGF-␤ in a similar way in Schwann cells and endoneurial fibroblasts of regenerating nerve. In the distal segment, NGF-␤ expression increased 4 d after injury, then fell markedly at the onset of regeneration at day 7, as shown previously (75).…”

Section: Discussionmentioning

confidence: 96%

Basement Membrane and Repair of Injury to Peripheral Nerve: Defining a Potential Role for Macrophages, Matrix Metalloproteinases, and Tissue Inhibitor of Metalloproteinases-1

Fleur

Underwood

Rappolee

et al. 1996

The Journal of Experimental Medicine

229

177

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Injury to a peripheral nerve is followed by a remodeling process consisting of axonal degeneration and regeneration. It is not known how Schwann cell–derived basement membrane is preserved after injury or what role matrix metalloproteinases (MMPs) and their inhibitors play in axonal degeneration and regeneration. We showed that the MMPs gelatinase B (MMP-9), stromelysin-1 (MMP-3), and the tissue inhibitor of MMPs (TIMP)-1 were induced in crush and distal segments of mouse sciatic nerve after injury. TIMP-1 inhibitor activity was present in excess of proteinase activity in extracts of injured nerve. TIMP-1 protected basement membrane type IV collagen from degradation by exogenous gelatinase B in cryostat sections of nerve in vitro. In vivo, during the early phase (1 d after crush) and later phase (4 d after crush) after injury, induction of TNF-α and TGF-β1 mRNAs, known modulators of TIMP-1 expression, were paralleled by an upregulation of TIMP-1 and gelatinase B mRNAs. At 4 days after injury, TIMP-1, gelatinase B, and TNF-α mRNAs were localized to infiltrating macrophages and Schwann cells in the regions of nerve infiltrated by elicited macrophages. TIMP-1 and cytokine mRNA expression was upregulated in undamaged nerve explants incubated with medium conditioned by macrophages or containing the cytokines TGF-β1, TNF-α, and IL-1α. These results show that TIMP-1 may protect basement membrane from uncontrolled degradation after injury and that cytokines produced by macrophages may participate in the regulation of TIMP-1 levels during nerve repair.

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Section: Discussionmentioning

confidence: 96%

Basement Membrane and Repair of Injury to Peripheral Nerve: Defining a Potential Role for Macrophages, Matrix Metalloproteinases, and Tissue Inhibitor of Metalloproteinases-1

Fleur

Underwood

Rappolee

et al. 1996

The Journal of Experimental Medicine

229

177

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“…One important action of proinflammatory cytokines is the regulation of gene expression. TNF (and IL-1) induce the expression of multiple cytokines, such as colony-stimulating factors, IL-2, IL-6, IL-8, hepatocyte growth factor, TGF-a, nerve growth factor, P-endorphin, and Gro-related factors (23,32,33,41,52,58,67,78). TNF has also been shown to induce IL-1 expression (27).…”

Section: Discussionmentioning

confidence: 99%

Signal Transduction by Tumor Necrosis Factor Mediated by JNK Protein Kinases

Sluss

Barrett

Dérijard

et al. 1994

Molecular and Cellular Biology

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JNK protein kinases are distantly related to mitogen-activated protein kinases (ERKs) and are activated by dual phosphorylation on Tyr and Thr. The JNK protein kinase group includes the 46-kDa isoform JNK1. Here we describe the molecular cloning of a second member of the JNK group, the 55-kDa protein kinase JNK2. The activities of both JNK isoforms are markedly increased by exposure of cells to UV radiation. Furthermore, JNK protein kinase activation is observed in cells treated with tumor necrosis factor. Although both JNK isoforms phosphorylate the NH2-terminal activation domain of the transcription factor c-Jun, the activity of JNK2 was approximately 10-fold greater than that of JNK1. This difference in c-Jun phosphorylation correlates with increased binding of c-Jun to JNK2 compared with JNK1. The distinct in vitro biochemical properties of these JNK isoforms suggest that they may have different functions in vivo. Evidence in favor of this hypothesis was obtained from the observation that JNK1, but not JNK2, complements a defect in the expression of the mitogen-activated protein kinase HOG1 in the yeast Saccharomyces cerevisiae. Together, these data indicate a role for the JNK group of protein kinases in the signal transduction pathway initiated by proinflammatory cytokines and UV radiation.

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“…TNF is produced in the CNS by neurons, astrocytes, and microglia 40 , and plays a prominent but paradoxical role in the brain because of its differential regulatory actions in healthy conditions versus during neurological disease or injury. TNF treatment on primary hippocampal neurons prevents hypoxia and NO-induced neuronal death 41 , ameliorates hippocampal damage in acute brain insults 42 and stimulates synthesis and secretion of nerve growth factors 43 . In addition to a role in neuroprotection, as mentioned above, TNF has emerged as a regulator of synaptic function in the hippocampus, such as the trafficking of GABA-A 44 and AMPA receptors 45 .…”

Section: Discussionmentioning

confidence: 99%

Pathway-specific TNF-mediated metaplasticity in hippocampal area CA1

Singh

Sateesh

Jones

et al. 2022

Sci Rep

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Long-term potentiation (LTP) is regulated in part by metaplasticity, the activity-dependent alterations in neural state that coordinate the direction, amplitude, and persistence of future synaptic plasticity. Previously, we documented a heterodendritic metaplasticity effect whereby high-frequency priming stimulation in stratum oriens (SO) of hippocampal CA1 suppressed subsequent LTP in the stratum radiatum (SR). The cytokine tumor necrosis factor (TNF) mediated this heterodendritic metaplasticity in wild-type rodents and in a mouse model of Alzheimer’s disease. Here, we investigated whether LTP at other afferent synapses to CA1 pyramidal cells were similarly affected by priming stimulation. We found that priming stimulation in SO inhibited LTP only in SR and not in a second independent pathway in SO, nor in stratum lacunosum moleculare (SLM). Synapses in SR were also more sensitive than SO or SLM to the LTP-inhibiting effects of pharmacological TNF priming. Neither form of priming was sex-specific, while the metaplasticity effects were absent in TNFR1 knock-out mice. Our findings demonstrate an unexpected pathway specificity for the heterodendritic metaplasticity in CA1. That Schaffer collateral/commissural synapses in SR are particularly susceptible to such metaplasticity may reflect an important control of information processing in this pathway in addition to its sensitivity to neuroinflammation under disease conditions.

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Tumor necrosis factor stimulates the synthesis and secretion of biologically active nerve growth factor in non-neuronal cells.

Cited by 145 publications

References 35 publications

Basement Membrane and Repair of Injury to Peripheral Nerve: Defining a Potential Role for Macrophages, Matrix Metalloproteinases, and Tissue Inhibitor of Metalloproteinases-1

Basement Membrane and Repair of Injury to Peripheral Nerve: Defining a Potential Role for Macrophages, Matrix Metalloproteinases, and Tissue Inhibitor of Metalloproteinases-1

Signal Transduction by Tumor Necrosis Factor Mediated by JNK Protein Kinases

Pathway-specific TNF-mediated metaplasticity in hippocampal area CA1

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