Tumor Necrosis Factor Receptor 2: Its Contribution to Acute Cellular Rejection and Clear Cell Renal Carcinoma

Wang, Jun; Al‐Lamki, Rafia S.

doi:10.1155/2013/821310

Cited by 27 publications

(31 citation statements)

References 94 publications

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“…TNFR2 does not contain a death domain, and therefore is not able to induce apoptosis through caspase-dependent mechanisms. Instead, TNFR2 promotes survival via phosphorylation of Etk and subsequent activation of Akt ( Figure I) [7,8].…”

Section: Tnf-a In Conditions Promoting Muscle Wastingmentioning

confidence: 99%

“…TNFR1 recruits TRADD and RIP1 prior to engaging with TRAF2, whereas TNFR2 can interact with TRAF2 directly [7]. TNFR1-triggered NF-kB activation leads to increased expression of muscle RING-finger protein 1 (MuRF1) and subsequent protein degradation through the ubiquitin proteasome pathway.…”

Section: Tnf-a In Conditions Promoting Muscle Wastingmentioning

confidence: 99%

“…The cytokine exerts its effect through two receptors, TNFR1 (p55) and TNFR2 (p75). TNFR1 is believed to mediate the muscle wasting effect, whereas TNFR2 is protective [6][7][8][9] (see Box 1 for details).…”

mentioning

confidence: 99%

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Cytokine Signaling in Skeletal Muscle Wasting

Zhou

Liu

Liang

et al. 2016

Trends in Endocrinology & Metabolism

148

104

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Section: Tnf-a In Conditions Promoting Muscle Wastingmentioning

confidence: 99%

Section: Tnf-a In Conditions Promoting Muscle Wastingmentioning

confidence: 99%

See 1 more Smart Citation

Cytokine Signaling in Skeletal Muscle Wasting

Zhou

Liu

Liang

et al. 2016

Trends in Endocrinology & Metabolism

148

104

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“…[1][2][3][4] TNF-a is a functional 26-kDa homotrimeric transmembrane protein, which is cleaved by a disintegrin and metalloprotease protein-17 (ADAM-17) and released into the circulation as a functional 17-kDa soluble form. 5 TNF-a mediates a lot of immunologic and inflammatory responses including the amplification of other proinflammatory cytokines and chemokines that contribute to local recruitment and activation of leucocytes. 6 TNF-a promotes T-cell activation, the key reaction leading to allograft rejection.…”

Section: Introductionmentioning

confidence: 99%

“…7 Binding of TNF-a to the TNFR1 or TNFR2 activates signaling pathways controlling inflammatory, immune and stress responses, as well as host defense and apoptosis. [5][6][7] In healthy subjects, TNF-a and TNFR2 are usually not present in the kidneys, whereas TNFR1 can be found in normal glomerular endothelium. 8,9 After stimulation (e.g., with lipopolysaccharide, interleukin (IL)-1a) and during inflammation, TNF-a and its receptors are expressed in glomerular and tubular cells.…”

Section: Introductionmentioning

confidence: 99%

Association between graft function and serum TNF-α, TNFR1 and TNFR2 levels in patients with kidney transplantation

Yılmaz

Akbaş

et al. 2015

Renal Failure

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Introduction: This prospective observational study aimed to assess the relevance of serial postoperative serum TNF-a, TNFR1 and TNFR2 measurements for predicting graft function and acute rejection episodes (AR) after transplantation. Materials and methods: We studied 50 kidney transplant recipients (31 female, 19 male; mean age: 38.36 ± 12.88). Blood samples were collected immediately before and after surgery at day 7, month 1 and month 3. Serum TNF-a, TNFR1 and TNFR2 levels were measured by ELISA using a commercial kit (Invitrogen ELISA). Serum cystatin-C levels were measured by particle-enhanced immunonephelometric method. Glomerular filtration rate (GFR) was estimated by Chronic Kidney Disease-Epidemiology (CKD-EPI) equation. Patients were assigned to their transplant outcomes in terms of acute rejection [AR(+) and AR(À)] and slow (SGF) or immediate graft function (IGF). Results: Among 50 recipients, six had AR(+) and 44 had AR(À), depending on graft function: 17 had SGF and 33 had IGF. Serum creatinine, cystatin-C, TNF-a, TNFR1 and TNFR2 levels demonstrated consistent significantly decreases after transplantation while GFR values had consistent increases (p ¼ 0.001). Pretransplant levels were not statistically different between AR(+) and AR(À) groups (TNF-a: 30.79 ± 5.96 vs. 27.95 ± 2.43 pg/mL, TNFR1: 55.96 ± 21.6 vs. 40.52 ± 7.41 ng/mL, TNFR2: 58.31 ± 8.06 vs. 50.9 ± 3.34 ng/mL, respectively) (p40.05). Serum TNF-a, TNFR1 and TNFR2 levels on day 7 and month 1 were also significantly higher in AR(+) group compared to AR(À) (p ¼ 0.012, p ¼ 0.049 for TNF-a, p ¼ 0.001, p ¼ 0.002 for TNFR1, p ¼ 0.001, p ¼ 0.002 for TNFR2). Conclusions: Our preliminary findings suggest that serum TNF-a, TNFR1 and TNFR2 levels might be considered useful markers of evaluating graft function after renal transplantation.

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Persistent astrocyte activation in the fragile X mouse cerebellum

et al. 2015

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BackgroundFragile X Syndrome, the most common single gene cause of autism, results from loss of the RNA‐binding protein FMRP. Although FMRP is highly expressed in neurons, it has also recently been identified in glia. It has been postulated that in the absence of FMRP, abnormal function of non‐neuronal cells may contribute to the pathogenesis of the disorder. We previously demonstrated reduced numbers of oligodendrocyte precursor cells and delayed myelination in the cerebellum of fragile X (Fmr1) knockout mice.MethodsWe used quantitative western blotting and immunocytochemistry to examine the status of astrocytes and microglia in the cerebellum of Fmr1 mice during development and in adulthood.ResultsWe report increased expression of the astrocyte marker GFAP in the cerebellum of Fmr1 mice starting in the second postnatal week and persisting in to adulthood. At 2 weeks postnatal, expression of Tumor Necrosis Factor Receptor 2 (TNFR2) and Leukemia Inhibitory Factor (LIF) were elevated in the Fmr1 KO cerebellum. In adults, expression of TNFR2 and the glial marker S100β were also elevated in Fmr1 knockouts, but LIF expression was not different from wild‐type mice. We found no evidence of microglial activation or neuroinflammation at any age examined.ConclusionsThese findings demonstrate an atypical pattern of astrogliosis in the absence of microglial activation in Fmr1 knockout mouse cerebellum. Enhanced TNFR2 and LIF expression in young mice suggests that changes in the expression of astrocytic proteins may be an attempt to compensate for delayed myelination in the developing cerebellum of Fmr1 mice.

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Tumor Necrosis Factor Receptor 2: Its Contribution to Acute Cellular Rejection and Clear Cell Renal Carcinoma

Cited by 27 publications

References 94 publications

Cytokine Signaling in Skeletal Muscle Wasting

Cytokine Signaling in Skeletal Muscle Wasting

Association between graft function and serum TNF-α, TNFR1 and TNFR2 levels in patients with kidney transplantation

Persistent astrocyte activation in the fragile X mouse cerebellum

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