An endogenous 55 kDa TNF receptor mediates cell death in a neural cell line

Sipe, Kimberly J.; Srisawasdi, Dalin; Dantzer, Robert; Kelley, Keith W.; Weyhenmeyer, James A.

doi:10.1016/0169-328x(95)00310-o

Cited by 59 publications

(36 citation statements)

References 30 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…TNF-␣ has been reported to inhibit glutamate uptake and has been shown to modulate the accumulation of extracellular glutamate by a pathway that involves the liberation of nitric oxide (45). In vitro, TNF-␣ has been observed to be cytotoxic to oligodendrocytes (14) and human or murine neurons (13,46) and may also participate in acute posttraumatic apoptotic and necrotic cell death (47), both of which have been associated with progressive regional cell death after brain trauma (48)(49)(50)(51)(52). In vivo, exogenous TNF-␣ has been shown to exacerbate focal ischemic injury in a dose-dependent manner if given shortly after the event (37).…”

Section: Discussionmentioning

confidence: 99%

Differential acute and chronic responses of tumor necrosis factor-deficient mice to experimental brain injury

Scherbel

Raghupathi

Nakamura

et al. 1999

Proc. Natl. Acad. Sci. U.S.A.

375

231

View full text Add to dashboard Cite

The present study evaluated behavioral and histopathological outcome after controlled cortical impact (CCI) brain injury in mice deficient in tumor necrosis factor [TNF(؊/؊)] and their wild-type (wt) littermates. Mice were subjected to CCI brain injury [TNF(؊/؊), n ‫؍‬ 10; wt, n ‫؍‬ 10] or served as uninjured controls [TNF(؊/؊), n ‫؍‬ 10; wt, n ‫؍‬ 10] and were evaluated for deficits in memory retention at 7 days postinjury. Although both brain-injured wt and TNF(؊/؊) mice exhibited significant memory dysfunction compared to uninjured controls (P < 0.02), the deficits in memory retention in injured TNF(؊/؊) mice were significantly less severe than in injured wt mice (P < 0.02). A second group of mice was subjected to CCI brain injury [TNF(؊/؊), n ‫؍‬ 20; wt, n ‫؍‬ 20] or served as uninjured controls [TNF(؊/؊), n ‫؍‬ 15; wt, n ‫؍‬ 15] and were evaluated over a 4-week period for neurological motor function. In the acute posttraumatic period (48 h postinjury), braininjured TNF(؊/؊) mice were significantly less impaired than injured wt mice on composite neuroscore (P < 0.001), rotarod (P < 0.05), and beam balance (P < 0.02) tests. However, wt mice recovered from brain injury by 2-3 weeks postinjury, whereas TNF(؊/؊) mice continued to demonstrate persistent motor deficits up to 4 weeks postinjury. Histopathological analysis at 2 and 4 weeks postinjury revealed that brain-injured TNF(؊/؊) mice had significantly more cortical tissue loss than wt mice (P < 0.02). Our results suggest that although the presence of TNF in the acute posttraumatic period may be deleterious, this cytokine may play a role in facilitating long-term behavioral recovery and histological repair after brain injury.

show abstract

Section: Discussionmentioning

confidence: 99%

Differential acute and chronic responses of tumor necrosis factor-deficient mice to experimental brain injury

Scherbel

Raghupathi

Nakamura

et al. 1999

Proc. Natl. Acad. Sci. U.S.A.

375

231

View full text Add to dashboard Cite

show abstract

“…Moreover, several studies have shown that A␤ induces the activity of NF-B DNA binding (Akama et al, 1998;Ghribi et al, 2001) and that NF-B is also reported to be TNFRI dependent not only in the peripheral immune system (Tartaglia et al, 1993;Hsu et al, 1995;Sipe et al, 1996), but also in the brain . To determine whether TNFRI is involved in the A␤ 1-40 -induced NF-B neuronal activity, an experiment for examining translocation of p65, a subunit of NF-B, was performed using Western blotting.…”

Section: Activated Nf-b Translocation By A␤ Is Diminished In Neurons mentioning

confidence: 99%

Tumor Necrosis Factor Death Receptor Signaling Cascade Is Required for Amyloid-β Protein-Induced Neuron Death

et al. 2004

View full text Add to dashboard Cite

Tumor necrosis factor type I receptor (TNFRI), a death receptor, mediates apoptosis and plays a crucial role in the interaction between the nervous and immune systems. A direct link between death receptor activation and signal cascade-mediated neuron death in brains with neurodegenerative disorders remains inconclusive. Here, we show that amyloid-␤ protein (A␤), a major component of plaques in the Alzheimer's diseased brain, induces neuronal apoptosis through TNFRI by using primary neurons overexpressing TNFRI by viral infection or neurons from TNFRI knock-out mice. This was mediated via alteration of apoptotic protease-activating factor (Apaf-1) expression that in turn induced activation of nuclear factor B (NF-B). A␤-induced neuronal apoptosis was reduced with lower Apaf-1 expression, and little NF-B activation was found in the neurons with mutated Apaf-1 or a deletion of TNFRI compared with the cells from wild-type (WT) mice. Our studies suggest a novel neuronal response of A␤, which occurs through a TNF receptor signaling cascade and a caspase-dependent death pathway.

show abstract

“…TNF-α is a proinflammatory and proapoptotic cytokine that can regulate cellular events and contribute to neuronal damage and functional impairment associated with SCI (Harrington et al, 2005) TNF-α level is elevated in human spinal cord after SCI, reaching a peak within 1 h after the initial trauma (Dinomais et al, 2009) and its expression is upregulated rapidly at the lesion site after SCI (Yan et al, 2001) leading to apoptosis of oligodendrocytes and neuronal cell line in vitro (Sipe et al, 1996). Rapid accumulation of TNF-α may act as an external signal initiating apoptosis after SCI in neurons and glial cells too (Li et al, 2000).…”

Section: Discussionmentioning

confidence: 99%

Effect of Bone Marrow-derived Mesenchymal Stem Cells on Changes of Serum Levels of TNF-α and Locomotor Function after Spinal Cord Injury in Mice

Gashmardi¹,

Mehrabani²,

Khodabande³

et al. 2015

J. of Medical Sciences

View full text Add to dashboard Cite

Spinal Cord Injury (SCI) is still a devastating clinical problem with irreversible consequences leading to permanent functional loss and life time disability. This study was conducted to assess the healing effect of bone marrow-derived mesenchymal stem cells on locomotor function and changes of Tumor Necrosis Factor alpha (TNF-α) after SCI in mice. Forty two BALB/C mice were divided into 3 equal groups of control, SCI and treatment [transplantation of 5×10 4 Bone Marrow Stem Cells (BMSCs)]. The SCI was induced by compression for 2 min at T10 and injury bilaterally. The femoral and tibial bones were used for bone marrow isolation and culture was made using Dulbecco's Modified Eagle's Medium supplemented with fetal bovine serum, L-glutamine and penicillin/streptomycin. Cell morphology was evaluated in all passages. Characterization of BMSCs was conducted by reverse transcription polymerase chain reaction and by osteogenic differentiation of BMSCs. The ELISA was undertaken for TNF-α. Open field locomotion was evaluated by Toyama mouse score. The BMSCs were plastic adherent and fibroblastic spindle-shape. MSCs were positive for CD90 and negative for CD34 and CD45. Osteogenic differentiation was noticed when stained with alizarin red. The serum TNF-α level increased after 24 h, 3 and 5 weeks post-SCI and was time dependent. The neurological score significantly improved after 8 weeks after BMSC transplantation. Transplantation of BMSCs was shown to decrease the TNF-α level and inflammation in injured spinal cord and improve the neurological outcome. These findings can be added to the literature for reduction of inflammation in SCI and improvement of neurological outcome after transplantation of BMSCs.

show abstract

An endogenous 55 kDa TNF receptor mediates cell death in a neural cell line

Cited by 59 publications

References 30 publications

Differential acute and chronic responses of tumor necrosis factor-deficient mice to experimental brain injury

Differential acute and chronic responses of tumor necrosis factor-deficient mice to experimental brain injury

Tumor Necrosis Factor Death Receptor Signaling Cascade Is Required for Amyloid-β Protein-Induced Neuron Death

Effect of Bone Marrow-derived Mesenchymal Stem Cells on Changes of Serum Levels of TNF-α and Locomotor Function after Spinal Cord Injury in Mice

Contact Info

Product

Resources

About