scholarly journals Changes in soluble tumor necrosis factor receptor type 1 levels and early renal function decline in patients with diabetes

2019 ◽  
Vol 10 (6) ◽  
pp. 1537-1542
Author(s):  
Richard J MacIsaac ◽  
Matthew Farag ◽  
Varuni Obeyesekere ◽  
Michele Clarke ◽  
Ray Boston ◽  
...  
Keyword(s):  
Renal Function ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Receptor ◽  
Receptor Type ◽  
Renal Function Decline ◽  
Patients With Diabetes ◽  
Necrosis Factor

The Role of Tumor Necrosis Factor Receptor Type 1 in Orthodontic Tooth Movement

2007 ◽  
Vol 86 (11) ◽  
pp. 1089-1094 ◽  
Author(s):  
I. Andrade ◽  
T.A. Silva ◽  
G.A.B. Silva ◽  
A.L. Teixeira ◽  
M.M. Teixeira
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tooth Movement ◽  
Tumor Necrosis Factor Receptor ◽  
Orthodontic Tooth Movement ◽  
Receptor Type ◽  
Periodontal Tissues ◽  
Tnf Α ◽  
Necrosis Factor

Orthodontic tooth movement is dependent on osteoclast activity. Tumor necrosis factor (TNF)-α plays an important role, directly or via chemokine release, in osteoclast recruitment and activation. This study aimed to investigate whether the TNF receptor type 1 (p55) influences these events and, consequently, orthodontic tooth movement. An orthodontic appliance was placed in wild-type mice (WT) and p55-deficient mice (p55−/−). Levels of TNF-α and 2 chemokines (MCP-1/CCL2, RANTES/CCL5) were evaluated in periodontal tissues. A significant increase in CCL2 and TNF-α was observed in both groups after 12 hrs of mechanical loading. However, CCL5 levels remained unchanged in p55−/− mice at this time-point. The number of TRAP-positive osteoclasts in p55−/− mice was significantly lower than that in WT mice. Also, there was a significantly smaller rate of tooth movement in p55−/− mice. Analysis of our data suggests that the TNFR-1 plays a significant role in orthodontic tooth movement that might be associated with changes in CCL5 levels.

scholarly journals Tumor Necrosis Factor Induces Tumor Necrosis via Tumor Necrosis Factor Receptor Type 1-Expressing Endothelial Cells of the Tumor Vasculature

2000 ◽  
Vol 156 (4) ◽  
pp. 1171-1176 ◽  
Author(s):  
Benjamin Stoelcker ◽  
Brigitte Ruhland ◽  
Thomas Hehlgans ◽  
Horst Bluethmann ◽  
Thomas Luther ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Receptor ◽  
Tumor Vasculature ◽  
Receptor Type ◽  
Necrosis Factor

scholarly journals Distinctive roles of tumor necrosis factor receptor type 1 and type 2 in a mouse disc degeneration model

2021 ◽  
Vol 31 ◽  
pp. 62-72
Author(s):  
Shanzheng Wang ◽  
Guodong Sun ◽  
Pan Fan ◽  
Lei Huang ◽  
Yaofei Chen ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Disc Degeneration ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Receptor ◽  
Receptor Type ◽  
Necrosis Factor

Polymorphisms of the tumor necrosis factor receptor type 1 locus among autoimmune susceptible and resistant inbred rat strains

2001 ◽  
Vol 53 (5) ◽  
pp. 427-429
Author(s):  
Takefumi Furuya ◽  
Jennifer L. Salstrom ◽  
Bina Joe ◽  
Akira Hashiramoto ◽  
David E. Dobbins ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Receptor ◽  
Receptor Type ◽  
Rat Strains ◽  
Inbred Rat Strains ◽  
Inbred Rat ◽  
Necrosis Factor

scholarly journals Expression of Nuclear Factor-κB, Tumor Necrosis Factor Receptor Type 1, and c-Myc in Human Astrocytomas

2001 ◽  
Vol 41 (4) ◽  
pp. 187-195 ◽  
Author(s):  
Shuji HAYASHI ◽  
Masaaki YAMAMOTO ◽  
Yushi UENO ◽  
Kohichi IKEDA ◽  
Koichi OHSHIMA ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Nuclear Factor Kappa B ◽  
Tumor Necrosis Factor Receptor ◽  
Receptor Type ◽  
Nuclear Factor ◽  
Nuclear Factor Kappa ◽  
Necrosis Factor ◽  
Human Astrocytomas

Microenvironmental Factors and The Role Of Tumor Necrosis Factor Receptor Type 1 (TNFR-1) In Chronic Lymphocytic Leukemia

Blood ◽  
2013 ◽  
Vol 122 (21) ◽  
pp. 4149-4149
Author(s):  
Claudia Duerr ◽  
Angela Schulz ◽  
Sibylle Ohl ◽  
Thorsten Zenz ◽  
Stephan Stilgenbauer ◽  
...  
Keyword(s):  
B Cells ◽  
Chronic Lymphocytic Leukemia ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Receptor ◽  
Lymphocytic Leukemia ◽  
Receptor Type ◽  
Tnf Α ◽  
Necrosis Factor

Abstract B-cell Chronic Lymphocytic Leukemia (CLL) represents the most common leukemia among adults in the western world and remains still incurable. CLL is characterized by the accumulation of malignant B-cells in the peripheral blood and the lymphoid organs due to apoptosis resistance. Removing the cells from their physiological microenvironment spontaneously drives them into apoptosis in vitro unless they are supported by bystander cells (e.g. stromal cells or accessory leukocytes) or soluble factors such as cytokines produced by these cells. In order to identify differences in the biology of healthy B-cells and the leukemic clones we performed comparative microarray analyses of both cell types before and after cultivation in high cell density that allows cell-cell interactions of CLL cells with accessory leukocytes. These studies revealed the establishment of an inflammatory microenvironment in CLL characterized by the transcriptional upregulation of several cytokines. Antibody array analyses of culture supernatants and blood serum samples confirmed the upregulation of these proteins and their relevance for CLL. The 11 most deregulated cytokines were quantified in the serum of 250 CLL patients of the German CLL8 study cohort and 50 age- and sex-matched controls in order to identify novel predictive or prognostic markers. Bioinformatical analyses of the data are currently ongoing. Among other proteins, we found Tumor Necrosis Factor Receptor Type 1 (TNFR-1) to be significantly upregulated in the malignant B-cells under survival-maintaining cultivation as well as in CLL serum, but not in healthy controls (Figure 1). To exploit the difference in TNFR-1 biology, we treated CLL cells with TNF-α in combination with wogonin which is known to block the survival supporting pathway propagated by TNFR-1 upon TNF-α binding. This combinational treatment strategy effectively triggered Disclosures: No relevant conflicts of interest to declare.

SOLUBLE TUMOR NECROSIS FACTOR RECEPTOR TYPE 1 LEVELS EXHIBIT A STRONGER ASSOCIATION WITH RENAL OUTCOMES THAN TRADITIONAL RISK FACTORS IN CHINESE SUBJECTS WITH TYPE 2 DIABETES MELLITUS

2020 ◽  
Vol 26 (10) ◽  
pp. 1115-1124
Author(s):  
Li-Hsin Chang ◽  
Chii-Min Hwu ◽  
Yi-Chun Lin ◽  
Chin-Chou Huang ◽  
Justin G.S. Won ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Diabetic Kidney Disease ◽  
Tumor Necrosis Factor Receptor ◽  
Receptor Type ◽  
Renal Outcomes ◽  
Necrosis Factor

Objective: Associations between albuminuria and renal outcomes are inconsistent in patients with type 2 diabetes (T2D). Soluble tumor necrosis factor receptor type 1 (sTNFR1) is involved in declined kidney function and poor renal outcomes but this has not been confirmed among Chinese T2D patients. This study aimed to examine the association of sTNFR1 and renal outcomes in a cohort of these patients. Methods: Two hundred and eighty-three Chinese T2D patients were enrolled in a prospective observational study which excluded individuals with estimated glomerular filtration rates (eGFR) <30 mL/min/1.73m2. Composite renal outcomes included either or both a >30% decline in eGFR and worsening albuminuria from consecutive tests of blood/urine during a 3.5-year follow-up. Results: Higher sTNFR1 levels were associated with impaired renal outcomes. sTNFR1 levels of ≥979 pg/mL yielded the most sensitivity and specific predictions of renal outcomes according to the receiver operating curve (area under the curve 0.68, P<.001; sensitivity 78.3%, specificity 48.9%). Renal events occurred more frequently in subjects with sTNFR1 ≥979 pg/mL than in others (sTNFR1 <979 pg/mL; 29% versus 10%; P<.001 by log-rank test). The association between sTNFR1 ≥979 pg/mL and renal outcomes remained significant after adjustment for relevant covariates (adjusted hazard ratio 2.43, 95% confidence interval 1.18 to 5.02; P = .01) and consistent across subgroups stratified by age, sex, blood pressure, eGFR, albuminuria, and the use of renin-angiotensin system inhibitors. Conclusion: Increased sTNFR1 levels were associated with renal outcomes in Chinese T2D subjects, making sTNFR1 a potential biomarker in diabetic kidney disease. Abbreviations: BMI = body mass index; CI = confidence interval; DKD = diabetic kidney disease; eGFR = estimated glomerular filtration rate; GLP-1a = glucagon-like peptide-1 agonist; HR = hazard ratio; RAS = reninangiotensin system; ROC = receiver operating characteristic; SGLT2i = inhibitors of the sodium glucose cotransporter; sTNFR1 = soluble tumor necrosis factor receptor type 1; T2D = type 2 diabetes; UACR = urinary albumin-creatinine ratio

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