Up-regulation of TNF-α in neurons of dorsal root ganglia and spinal cord during coronary artery occlusion in rats

Niu, Yan-Lan; Guo, Zheng; Zhou, Raorao

doi:10.1016/j.cyto.2009.04.003

Cited by 18 publications

(13 citation statements)

References 45 publications

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“…TNF-α activates various signaling pathways in immune cells, neurons, epithelial cells, and adipocytes [14]–[16]. TNF-α signaling can have destructive or protective effects on target cells depending on the expression of its receptors and downstream signaling components [25]–[28].…”

Section: Discussionmentioning

confidence: 99%

“…TNF-α and its receptors are known to regulate a variety of cellular signaling pathways that affect cell growth, proliferation, differentiation, and survival [13]. TNF-α was thought to be produced primarily by macrophages, but it is also produced by a broad variety of cell types, including lymphoid cells, mast cells, endothelial cells, cardiac myocytes, adipocytes, fibroblasts, and neurons [14]–[16]. In the oral cavity, TNF-α has been found in salivary glands and saliva [17]–[19].…”

Section: Introductionmentioning

confidence: 99%

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Expression and Secretion of TNF-α in Mouse Taste Buds: A Novel Function of a Specific Subset of Type II Taste Cells

et al. 2012

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Taste buds are chemosensory structures widely distributed on the surface of the oral cavity and larynx. Taste cells, exposed to the oral environment, face great challenges in defense against potential pathogens. While immune cells, such as T-cells and macrophages, are rarely found in taste buds, high levels of expression of some immune-response-associated molecules are observed in taste buds. Yet, the cellular origins of these immune molecules such as cytokines in taste buds remain to be determined. Here, we show that a specific subset of taste cells selectively expresses high levels of the inflammatory cytokine tumor necrosis factor-α (TNF-α). Based on immuno-colocalization experiments using taste-cell-type markers, the TNF-α-producing cells are predominantly type II taste cells expressing the taste receptor T1R3. These cells can rapidly increase TNF-α production and secretion upon inflammatory challenges, both in vivo and in vitro. The lipopolysaccharide (LPS)-induced TNF-α expression in taste cells was completely eliminated in TLR2−/−/TLR4−/− double-gene-knockout mice, which confirms that the induction of TNF-α in taste buds by LPS is mediated through TLR signaling pathways. The taste-cell-produced TNF-α may contribute to local immune surveillance, as well as regulate taste sensation under normal and pathological conditions.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Expression and Secretion of TNF-α in Mouse Taste Buds: A Novel Function of a Specific Subset of Type II Taste Cells

et al. 2012

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“…TNF was thought to be produced primarily by macrophages, but it is also produced by a broad variety of cell types including lymphoid cells, mast cells, endothelial cells, cardiac myocytes, fibroblasts, adipocytes, and neurons (Hotamisligil et al, 1993; Niu et al, 2009; Walsh et al, 1991). TNF is known to activate a variety of cellular signaling pathways that are important not only for fighting against certain pathogens but also for regulating stress responses and metabolism (Cabal-Hierro and Lazo, 2012; Silke, 2011; Wajant et al, 2003).…”

Section: Introductionmentioning

confidence: 99%

Regulation of bitter taste responses by tumor necrosis factor

Feng

Jyotaki

Kim

et al. 2015

Brain, Behavior, and Immunity

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Inflammatory cytokines are important regulators of metabolism and food intake. Over production of inflammatory cytokines during bacterial and viral infections leads to anorexia and reduced food intake. However, it remains unclear whether any inflammatory cytokines are involved in the regulation of taste reception, the sensory mechanism governing food intake. Previously, we showed that tumor necrosis factor (TNF), a potent proinflammatory cytokine, is preferentially expressed in a subset of taste bud cells. The level of TNF in taste cells can be further induced by inflammatory stimuli. To investigate whether TNF plays a role in regulating taste responses, in this study, we performed taste behavioral tests and gustatory nerve recordings in TNF knockout mice. Behavioral tests showed that TNF-deficient mice are significantly less sensitive to the bitter compound quinine than wild-type mice, while their responses to sweet, umami, salty, and sour compounds are comparable to those of wild-type controls. Furthermore, nerve recording experiments showed that the chorda tympani nerve in TNF knockout mice is much less responsive to bitter compounds than that in wild-type mice. Chorda tympani nerve responses to sweet, umami, salty, and sour compounds are similar between TNF knockout and wild-type mice, consistent with the results from behavioral tests. We further showed that taste bud cells express the two known TNF receptors TNFR1 and TNFR2 and, therefore, are potential targets of TNF. Together, our results suggest that TNF signaling preferentially modulates bitter taste responses. This mechanism may contribute to taste dysfunction, particularly taste distortion, associated with infections and some chronic inflammatory diseases.

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“…TNF-α plays a pivotal role in CCI and sciatica-related nociception (1) and is upregulated in DRG neurons following spinal cord injury (2). It has been reported that HMGB1 is released from activated macrophages partly in a TNF-dependent manner (14).…”

Section: Discussionmentioning

confidence: 99%

“…Human herniated discs have been shown to express a number of pro-inflammatory mediators, including tumor necrosis factor-α (TNF-α), interleukin-1 (IL-1), IL-6 and IL-8 (1). TNF-α and its receptor are reportedly upregulated in dorsal root ganglion (DRG) neurons following lumbar injury in rats (2,3). The application of recombinant TNF-α to the lumbar nerve roots of rodents induces mechanical allodynia and hyperalgesia (1).…”

Section: Introductionmentioning

confidence: 99%

Etanercept decreases HMGB1 expression in dorsal root ganglion neuron cells in a rat chronic constriction injury model

Wang

Zhang

Pan

et al. 2012

Experimental and Therapeutic Medicine

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In the present study, we examined the effect of etanercept on high mobility group box 1 (HMGB1) expression in dorsal root ganglion (DRG) neuron cells in a rat model of chronic constriction injury (CCI) of the sciatic nerve, with the aim of exploring the molecular mechanism underlying the therapeutic effect of etanercept on sciatica-related nociception and the potential interaction between tumor necrosis factor-α (TNF-α) and HMGB1 in DRG neuron cells. A rat CCI model was employed and the animals were randomly assigned to seven groups (n=20/group): untreated, sham only, sham/saline, sham/etanercept, CCI only, CCI/saline and CCI/etanercept. Our results revealed that compared with the sham/saline and sham/etanercept groups, thermal hyperalgesia and mechanical hyperalgesia, as well as HMGB1 expression at both the mRNA and protein levels in the DRG neuron cells, were induced by CCI, and were significantly inhibited by etanercept. Although etanercept showed no significant effect on the sham group, it significantly reduced the phosphorylated p38 mitogen-activated protein kinase (MAPK) levels induced by CCI in the DRG neuron cells. In conclusion, we demonstrated that etanercept significantly decreased the HMGB1 expression induced by CCI in the DRG neuron cells. This study not only explored the molecular mechanisms underlying the therapeutic effect of etanercept on sciatica-related nociception, but also provided indirect evidence for an interaction between TNF-α and HMGB1 in DRG neuron cells.

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Up-regulation of TNF-α in neurons of dorsal root ganglia and spinal cord during coronary artery occlusion in rats

Cited by 18 publications

References 45 publications

Expression and Secretion of TNF-α in Mouse Taste Buds: A Novel Function of a Specific Subset of Type II Taste Cells

Expression and Secretion of TNF-α in Mouse Taste Buds: A Novel Function of a Specific Subset of Type II Taste Cells

Regulation of bitter taste responses by tumor necrosis factor

Etanercept decreases HMGB1 expression in dorsal root ganglion neuron cells in a rat chronic constriction injury model

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