Histamine Antagonizes Tumor Necrosis Factor (TNF) Signaling by Stimulating TNF Receptor Shedding from the Cell Surface and Golgi Storage Pool

Wang, Jun; Al‐Lamki, Rafia S.; Zhang, Hui; Kirkiles-Smith, Nancy C.; Gaeta, Mary Lou; Thiru, S; Pober, Jordan S.; Bradley, John R.

doi:10.1074/jbc.m212662200

Cited by 78 publications

(85 citation statements)

References 47 publications

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“…Samples were centrifuged, and the supernatants were collected and boiled in sample buffer (75 mM Tris/HCl, 10% sucrose, 0.2 mg/ml bromphenol blue, and 2% SDS) for 3 min before analysis by immunoblotting as described previously. 24 Rabbit polyclonal anti-IkB-␣ antibody (Santa Cruz Biotechnology, Santa Cruz, CA) or rabbit polyclonal anti-cleaved caspase-3 (Asp175; Cell Signaling Technology) were used at a dilution of 1:1000 and detected by enhanced chemiluminescence using ECL according to the manufacturer's instructions.…”

Section: Detection Of I B-␣ Degradation or Cleaved Caspase-3 In Humanmentioning

confidence: 99%

TL1A Both Promotes and Protects from Renal Inflammation and Injury

Al‐Lamki¹,

Wang²,

Tolkovsky

et al. 2008

Journal of the American Society of Nephrology

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Death receptor 3 (DR3), a member of the TNF receptor (TNFR) superfamily, is induced in human renal tubular epithelial cells (TEC) in response to injury. This study examined the expression and actions of TL1A, the principal ligand for DR3. In histologically normal tissue from biopsy or nephrectomy specimens of renal allografts, TL1A mRNA and protein were expressed in vascular endothelial cells but not in TEC. In specimens of acute or antibody-mediated allograft rejection, vascular endothelial cells and infiltrating leukocytes expressed increased TL1A mRNA and protein, but TEC expressed TL1A protein without mRNA, consistent with uptake of exogenous ligand. Addition of TL1A to organ cultures of human or mouse kidney caused activation of NF-B, expression of TNFR2, activation of caspase-3, and apoptosis in TEC. Inhibition of NF-B activation increased TL1A-mediated caspase-3 activation and apoptosis of TEC, but it did not reduce the induction of TNFR2. In organ culture of DR3-deficient mouse kidneys, addition of TL1A induced TNFR2 but did not activate NF-B and did not increase apoptosis of TEC. These data suggest that TL1A may contribute to renal inflammation and injury through DR3-mediated activation of NF-B and caspase-3, respectively, but that an unidentified receptor may mediate the NF-B-independent induction of TNFR2 in TEC.

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Section: Detection Of I B-␣ Degradation or Cleaved Caspase-3 In Humanmentioning

confidence: 99%

TL1A Both Promotes and Protects from Renal Inflammation and Injury

Al‐Lamki¹,

Wang²,

Tolkovsky

et al. 2008

Journal of the American Society of Nephrology

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“…The present results are consistent with preincubation of LECs with apoA-I before TNF treatment reducing total TNF-R1 expression, including the receptor molecules at the cell surface, which confer cellular sensitivity to TNF, and in the Golgi, which is responsible for replenishing cell surface TNF-R1 levels. 17 Several lines of evidence were consistent with reduced TNF-R1 signaling in LECs that were preincubated with apoA-I. These include reduced TNF-R-associated factor 2 mRNA levels, reduced phosphorylation of p38 MAPK, and partial recovery of Lyve-1 expression.…”

Section: Discussionmentioning

confidence: 69%

“…We then wanted to find whether the ability of apoA-I to limit the bioactivity of TNF reflected reduced the expression of the endothelial receptor TNF-R1. 16,17 TNF-R1 mRNA levels in LECs were not affected by incubation with TNF alone ( Figure 5A). However, when the LECs were preincubated with apoA-I before activation with TNF, TNF-R1 mRNA levels were 2.3-fold lower than those in control cells (P<0.01) and 1.8-fold lower than those in cells that were incubated with TNF alone (P<0.05; Figure 5A).…”

Section: Tnf-r1 Mrna Levels In Lecsmentioning

confidence: 95%

“…This sheddase regulates cellular responsiveness to TNF by releasing soluble TNF-R1 from the cell surface, which inactivates TNF. 17 The possibility that TACE-mediated cleavage was responsible for the reduced TNF-R1 expression was addressed by using flow cytometry to quantify TACE expression in LECs. After preincubation with apoA-I, the number of TACE-expressing LECs was increased by 1.4-fold relative to LECs that were incubated with TNF alone (P<0.05; Figure V in the online-only Data Supplement).…”

Section: Preincubation With Apoa-i Increases Tnf-α-converting Enzyme mentioning

confidence: 99%

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Apolipoprotein A-I Limits the Negative Effect of Tumor Necrosis Factor on Lymphangiogenesis

Bisoendial

Tabet

Tak

et al. 2015

ATVB

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Objective— Lymphatic endothelial dysfunction underlies the pathogenesis of many chronic inflammatory disorders. The proinflammatory cytokine tumor necrosis factor (TNF) is known for its role in disrupting the function of the lymphatic vasculature. This study investigates the ability of apolipoprotein (apo) A-I, the principal apolipoprotein of high-density lipoproteins, to preserve the normal function of lymphatic endothelial cells treated with TNF. Approach and Results— TNF decreased the ability of lymphatic endothelial cells to form tube-like structures. Preincubation of lymphatic endothelial cells with apoA-I attenuated the TNF-mediated inhibition of tube formation in a concentration-dependent manner. In addition, apoA-I reversed the TNF-mediated suppression of lymphatic endothelial cell migration and lymphatic outgrowth in thoracic duct rings. ApoA-I also abrogated the negative effect of TNF on lymphatic neovascularization in an ATP-binding cassette transporter A1-dependent manner. At the molecular level, this involved downregulation of TNF receptor-1 and the conservation of prospero-related homeobox gene-1 expression, a master regulator of lymphangiogenesis. ApoA-I also re-established the normal phenotype of the lymphatic network in the diaphragms of human TNF transgenic mice. Conclusions— ApoA-I restores the neovascularization capacity of the lymphatic system during TNF-mediated inflammation. This study provides a proof-of-concept that high-density lipoprotein–based therapeutic strategies may attenuate chronic inflammation via its action on lymphatic vasculature.

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“…5 Similarly to tmTNF itself, both TNF receptors can be cleaved by TACE into soluble TNF-Rs that can neutralize the TNF activity. 6,7 Whereas tmTNF binds both receptors, sTNF preferentially binds to TNF-R1. The differences in the intracellular domain as well as the preferential binding of sTNF to TNF-R1 may lead to different biological effects of both receptors as demonstrated by different experimental models.…”

mentioning

confidence: 99%

Relative Expression of Soluble tnf Versus Transmembrane tnf in Spondyloarthritis

Masdar¹

2017

JIK

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TNF is important in rheumatoid arthritis (RA) and spondyloarthritis (SpA) pathogenesis. Recently reports showedsTNF levels were significantly lower in SpA than RA synovial fluid (SF). Therefore, the differential regulation of TNFin both diseases were investigated focusing on the balance of sTNF-tmTNF and both TNF receptors expression. Synovialfluid from 22 RA and 25 SpA were analyzed by ELISA. sTNF was confirmed significantly higher in RA than SpA.Total TNF of synovial tissues assessed by qPCR showed similar levels, suggesting a higher tmTNF/sTNF ratio in SpA.The levels of sTNF-R1 and sTNF-R2 were significantly lower in SpA than RA SF. Interestingly, sTNF-R2/sTNF-R1increased in SpA. qPCR on synovial tissue showed similar mRNA levels for TNF-R2 but decrease of TNF-R1 in SpA.IL-6R levels did not showed differences and TIMP-3 tended to be higher in RA than in SpA SF. In conclusion, weobserved a shift from sTNF/TNF-R1 in RA to tmTNF/TNF-R2 in SpA.

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Histamine Antagonizes Tumor Necrosis Factor (TNF) Signaling by Stimulating TNF Receptor Shedding from the Cell Surface and Golgi Storage Pool

Abstract: Tumor necrosis factor (TNF) activates pro-inflammatory functions of vascular endothelial cells (EC) through

Cited by 78 publications

References 47 publications

TL1A Both Promotes and Protects from Renal Inflammation and Injury

TL1A Both Promotes and Protects from Renal Inflammation and Injury

Apolipoprotein A-I Limits the Negative Effect of Tumor Necrosis Factor on Lymphangiogenesis

Relative Expression of Soluble tnf Versus Transmembrane tnf in Spondyloarthritis

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