scholarly journals Levels of Tumor Necrosis Factor-α (TNF-α) and Transforming Growth Factor-β1 (TGF-β1) in Gingival Crevicular Fluid During Canine Retraction Using Elastic Chain and Closed Coil Spring

2018 ◽  
Vol 9 (2) ◽  
pp. 31
Author(s):  
AnantoA Alhasyimi ◽  
Sri Suparwitri ◽  
Wahyu Hidayat ◽  
H. Hendrawati
Keyword(s):  
Transforming Growth Factor ◽  
Gingival Crevicular Fluid ◽  
Transforming Growth Factor Β1 ◽  
Coil Spring ◽  
Canine Retraction ◽  
Tnf Α ◽  
Factor Α ◽  
Crevicular Fluid ◽  
Tgf Β1 ◽  
Necrosis Factor

scholarly journals Tumor Necrosis Factor–α Levels during Two Different Canine Distalization Techniques

2007 ◽  
Vol 77 (1) ◽  
pp. 142-147 ◽  
Author(s):  
Seniz Karacay ◽  
Işıl Saygun ◽  
Ali Osman Bengi ◽  
Muhittin Serdar
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Gingival Crevicular Fluid ◽  
Tissue Response ◽  
Hybrid Reactor ◽  
Tnf Α ◽  
Factor Α ◽  
Crevicular Fluid ◽  
Canine Distalization ◽  
Necrosis Factor

Abstract Objectives: To compare levels of tumor necrosis factor (TNF)-α while applying continuous and heavy interrupted forces. Materials and Methods: A hybrid retractor was used in the first group. In the second group, rapid canine distalization through periodontal distraction was performed. Gingival crevicular fluid samples were collected from the distal sides of the canine teeth before attaching the appliances and at 1 hour, 24 hours, and 1 week after the force was applied. Results: In the hybrid reactor group, concentration of TNF-α decreased at 1 week according to 24-hour measurements. In the rapid canine distalization group, it severely increased at 1 hour. In the evaluation of between-group differences, significantly higher values were determined in the rapid canine distalization group at 1 hour and 1 week. Conclusions: Heavy interrupted force induces a rapid release of TNF-α, and the tissue response continues for a longer time period. To avoid the harmful effects of heavy interrupted force, there might be feedback mechanisms that prevent the mediators from increasing excessively.

Synergistic induction of nuclear factor-κB by transforming growth factor-β and tumour necrosis factor-α is mediated by protein kinase A-dependent RelA acetylation

2008 ◽  
Vol 417 (2) ◽  
pp. 583-591 ◽  
Author(s):  
Hajime Ishinaga ◽  
Hirofumi Jono ◽  
Jae Hyang Lim ◽  
Kensei Komatsu ◽  
Xiangbin Xu ◽  
...  
Keyword(s):  
Transforming Growth Factor ◽  
Inflammatory Responses ◽  
Transforming Growth Factor Β ◽  
Nuclear Factor Κb ◽  
Binding Activity ◽  
Dna Binding Activity ◽  
Tnf Α ◽  
Factor Α ◽  
Tgf Β1 ◽  
Necrosis Factor

The TGF-β (transforming growth factor-β) pathway represents an important signalling pathway involved in regulating diverse biological processes, including cell proliferation, differentiation and inflammation. Despite the critical role for TGF-β in inflammatory responses, its role in regulating NF-κB (nuclear factor-κB)-dependent inflammatory responses still remains unknown. In the present study we show that TGF-β1 synergizes with proinflammatory cytokine TNF-α (tumour necrosis factor-α) to induce NF-κB activation and the resultant inflammatory response in vitro and in vivo. TGF-β1 synergistically enhances TNF-α-induced NF-κB DNA binding activity via induction of RelA acetylation. Moreover, synergistic enhancement of TNF-α-induced RelA acetylation and DNA-binding activity by TGF-β1 is mediated by PKA (protein kinase A). Thus the present study reveals a novel role for TGF-β in inflammatory responses and provides new insight into the regulation of NF-κB by TGF-β signalling.

Polymorphisms in TGFβ and TNFα Are Associated With the Myelodysplastic Syndrome Phenotype

2007 ◽  
Vol 131 (12) ◽  
pp. 1789-1793 ◽  
Author(s):  
Martin P. Powers ◽  
Ha Nishino ◽  
Yamin Luo ◽  
Alina Raza ◽  
Amulya Vanguri ◽  
...  
Keyword(s):  
Transforming Growth Factor ◽  
Transforming Growth Factor Β ◽  
Aberrant Expression ◽  
Genotype Frequencies ◽  
Tnf Α ◽  
Genes Encoding ◽  
Primer Polymerase Chain Reaction ◽  
Factor Α ◽  
Tgf Β1 ◽  
Necrosis Factor

Abstract Context.—Myelodysplastic syndromes (MDSs) are characterized by ineffective hematopoiesis, excessive apoptosis, and the aberrant expression of a number of cytokines. The genes encoding these cytokines are significantly polymorphic. It is unknown whether these cytokine polymorphisms are associated with, and may therefore be playing a role in the pathogenesis of, MDS. Objective.—To determine if certain polymorphisms in the tumor necrosis factor α (TNF-α) and transforming growth factor β (TGF-β) cytokines are overrepresented in a cohort of patients with MDSs. Design.—DNA was isolated from the peripheral blood or bone marrow aspirate of 21 patients with MDS. The genotypes for 4 different polymorphisms, 2 in TNFα and 2 in TGFβ1, were determined using single-specific-primer polymerase chain reaction. The allele and genotype frequencies were compared with similar populations in the National Cancer Institute SNP500 database. Results.—In our MDS population, the −308A/A genotype of the TNFα gene and the TGFβ1 allele +29T and genotype +29T/T, each associated with higher levels of expression, were overrepresented in our MDS population. Conclusions.—Polymorphisms associated with increased expression in the cytokines TNFα and TGFβ1 are overrepresented in the MDS population suggesting that increased TNF-α and TGF-β1 activity may contribute to the susceptibility and/or pathogenesis of MDS. Further studies with larger sample sizes are warranted to confirm our observation.

Localization of cyclooxygenase-2 and regulation of its mRNA expression in gastric ulcers in rats

1998 ◽  
Vol 275 (5) ◽  
pp. G1137-G1145 ◽  
Author(s):  
Satoru Takahashi ◽  
Jun-Ichi Shigeta ◽  
Hiroyasu Inoue ◽  
Tadashi Tanabe ◽  
Susumu Okabe
Keyword(s):  
Mrna Expression ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β1 ◽  
Cyclooxygenase 2 ◽  
Gastric Ulcers ◽  
Tnf Α ◽  
Ulcer Base ◽  
Cox 2 ◽  
Factor Α ◽  
Tgf Β1

It has been reported that cyclooxygenase-2 (COX-2) may play a crucial role in gastric ulcer healing. We examined the localization of COX-2 and the regulation of COX-2 mRNA expression in acetic acid ulcers in rats. PGE2 production was elevated in ulcerated tissue but not in intact tissue. COX-2 mRNA expression was induced in only the ulcerated tissue, and COX-2 protein was found in fibroblasts, monocytes/macrophages, and granulocytes. A selective COX-2 inhibitor inhibited increased PGE2 production by the ulcerated tissue. Interleukin-1β (IL-1β), tumor necrosis factor-α (TNF-α), and transforming growth factor-β1 (TGF-β1) mRNAs were also expressed only in the ulcerated tissue. In a culture of isolated ulcer base, blockade of IL-1β and TNF-α reduced COX-2 mRNA expression and PGE2 production. In contrast, COX-2 mRNA expression and PGE2 production were promoted by prevention of TGF-β1 action. These results indicate that COX-2 protein is highly localized in the base of gastric ulcers in rats and that COX-2 mRNA expression might be regulated positively by IL-1β and TNF-α and negatively by TGF-β1.

Regulation of extracellular matrix synthesis by TNF-α and TGF-β1 in type II cells exposed to coal dust

1998 ◽  
Vol 275 (4) ◽  
pp. L637-L644 ◽  
Author(s):  
Yu-Chen Lee ◽  
D. Eugene Rannels
Keyword(s):  
Extracellular Matrix ◽  
Cell Cultures ◽  
Transforming Growth Factor ◽  
Coal Dust ◽  
Transforming Growth Factor Β1 ◽  
Type Ii ◽  
Tnf Α ◽  
Type Ii Cell ◽  
Primary Type ◽  
Tgf Β1

Type II pulmonary epithelial cells respond to anthracite coal dust PSOC 867 with increased synthesis of extracellular matrix (ECM) components. Alveolar macrophages modulate this response by pathways that may involve soluble mediators, including tumor necrosis factor-α (TNF-α) or transforming growth factor-β1 (TGF-β1). The effects of TNF-α (10 ng/ml) and/or TGF-β1 (2 ng/ml) were thus investigated in dust-exposed primary type II cell cultures. In control day 1 or day 3 cultures, TNF-α and/or TGF-β1 had little or no effect on the synthesis of type II cellular proteins, independent of whether the cells were exposed to dust. With PSOC 867 exposure, where ECM protein synthesis is elevated, TNF-α and TGF-β1 further increased both the absolute and relative rates of ECM synthesis on day 3 but had little effect on day 1. Each mediator increased expression of fibronectin mRNA, as well as of ECM fibronectin content, in a manner qualitatively similar to their effects on synthesis. Thus TNF-α and TGF-β1 modulate both ECM synthesis and fibronectin content in coal dust-exposed type II cell cultures.

Contributions of angiotensin II and tumor necrosis factor-α to the development of renal fibrosis

2001 ◽  
Vol 280 (5) ◽  
pp. F777-F785 ◽  
Author(s):  
Guangjie Guo ◽  
Jeremiah Morrissey ◽  
Ruth McCracken ◽  
Timothy Tolley ◽  
Helen Liapis ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Tumor Necrosis Factor ◽  
Renal Fibrosis ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Wild Type ◽  
Tnf Α ◽  
Factor Α ◽  
Tgf Β1 ◽  
Necrosis Factor

Angiotensin II upregulates tumor necrosis factor-α (TNF-α) in the rat kidney with unilateral ureteral obstruction (UUO). In a mouse model of UUO, we found that tubulointerstitial fibrosis is blunted when the TNF-α receptor, TNFR1, is functionally knocked out. In this study, we used mutant mice with UUO in which the angiotensin II receptor AT1a or the TNF-α receptors TNFR1 and TNFR2 were knocked out to elucidate interactions between the two systems. The contribution of both systems to renal fibrosis was assessed by treating TNFR1/TNFR2-double knockout (KO) mice with an angiotensin-converting enzyme inhibitor, enalapril. The increased interstitial volume (Vvint) in the C57BI/6 wild-type mouse was decreased in the AT1a KO from 32.8 ± 4.0 to 21.0 ± 3.7% ( P < 0.005) or in the TNFR1/TNFR2 KO to 22.3 ± 2.1% ( P < 0.005). The Vvint of the TNFR1/TNFR2 KO was further decreased to 15.2 ± 3.7% ( P < 0.01) by enalapril compared with no treatment. The induction of TNF-α mRNA and transforming growth factor-β1 (TGF-β1) mRNA in the kidney with UUO was significantly blunted in the AT1a or TNFR1/TNFR2 KO mice compared with the wild-type mice. Treatment of the TNFR1/TNFR2 KO mouse with enalapril reduced both TNF-α and TGF-β1 mRNA and their proteins to near normal levels. Also, α-smooth muscle actin expression and myofibroblast proliferation were significantly inhibited in the AT1a or TNFR1/TNFR2 KO mice, and they were further inhibited in enalapril-treated TNFR1/TNFR2 KO mice. Incapacitating the angiotensin II or the TNF-α systems individually leads to partial blunting of fibrosis. Incapacitating both systems, by using a combination of genetic and pharmacological means, further inhibited interstitial fibrosis and tubule atrophy in obstructive nephropathy.

Exposure to febrile temperature modifies endothelial cell response to tumor necrosis factor-α

2001 ◽  
Vol 90 (1) ◽  
pp. 90-98 ◽  
Author(s):  
Jeffrey D. Hasday ◽  
Douglas Bannerman ◽  
Sirhan Sakarya ◽  
Alan S. Cross ◽  
Ishwar S. Singh ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β ◽  
Gm Csf ◽  
Tnf Α ◽  
Neutrophil Adherence ◽  
Endothelial Cell Response ◽  
Factor Α ◽  
Necrosis Factor

Fever is an important regulator of inflammation that modifies expression and bioactivity of cytokines, including tumor necrosis factor (TNF)-α. Pulmonary vascular endothelium is an important target of TNF-α during the systemic inflammatory response. In this study, we analyzed the effect of a febrile range temperature (39.5°C) on TNF-α-stimulated changes in endothelial barrier function, capacity for neutrophil binding and transendothelial migration (TEM), and cytokine secretion in human pulmonary artery endothelial cells (EC). Permeability for [14C]BSA tracer was increased by treatment with TNF-α, and this effect was augmented by incubating EC at 39.5°C. Treating EC with 2.5 U/ml TNF-α stimulated an increase in subsequent neutrophil adherence and TEM. Incubating EC at 39.5°C caused a 30% increase in TEM but did not modify the enhancement of neutrophil adherence or TEM by TNF-α treatment. Analysis of cytokine expression in EC cultures exposed to TNF-α at either 37° or 39.5°C revealed three patterns of temperature and TNF-α responsiveness. Granulocyte-macrophage colony stimulating factor (GM-CSF) and interleukin (IL)-8 were not detectable in untreated EC but were increased after TNF-α exposure, and this increase was enhanced at 39.5°C. IL-6 expression was also increased with TNF-α exposure, but IL-6 expression was lower in 39.5°C EC cultures. Transforming growth factor-β1was constitutively expressed, and its expression was not influenced either by TNF-α or exposure to 39.5°C. These data demonstrate that clinically relevant shifts in body temperature might cause important changes in the effects of proinflammatory cytokines on the endothelium.

The Possible Protective Effect of Selenium on Liver Dysfunction in a Rat Model of Extrahepatic Cholestasis

QJM ◽  
2021 ◽  
Vol 114 (Supplement_1) ◽  
Author(s):  
Fatma M Lebda ◽  
Sahar M El Agaty ◽  
Noha A Nassef ◽  
Marina A Aziz
Keyword(s):  
Bile Duct ◽  
Transforming Growth Factor ◽  
Group Versus ◽  
Serum Levels ◽  
Selenium Supplementation ◽  
Necrosis Factor Alpha ◽  
Tnf Α ◽  
Factor Alpha ◽  
Tgf Β1 ◽  
Necrosis Factor

Abstract Background Oxidative stress and inflammation are primarily implicated in the development and progression of liver injury during cholestasis. Selenium, a known essential antioxidant trace element, was found to provide a remarkable antioxidant and anti-inflammatory effects on various diseases. Aim This study was planned to evaluate the possible protective effect of selenium supplementation in a rat model of chronic cholestasis. Design Experimental study. Methods This study was carried out on adult male rats allocated randomly into sham, bile duct ligated (BDL), and BDL-selenium treated (BDL-Se) groups. Sodium selenite was given by gavage daily, in a dose of 100 µg/kg for 6 weeks, starting 2 weeks before the BDL. Results BDL group presented a significant increase in serum levels of aspartate aminotransferase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), and liver levels of malondialdehyde (MDA), tumor necrosis factor alpha (TNF-α), and transforming growth factor beta 1(TGF-β1), associated with a significant decrease in serum levels of total proteins (TP) compared to sham group . Selenium supplementation significantly lowered serum levels of AST, ALT, ALP, and liver levels of MDA, TNF-α, and TGF-β1 along with a significant increase in serum TP in BDL-Se group versus BDL rats. Histological analysis of liver showed a significant attenuation of the inflammatory score and a significant decrease in the percentage area of collagen deposition in BDL-Se group versus BDL rats. Conclusion Selenium supplementation reduces liver injury and improves liver functions in experimental cholestasis probably by its antioxidant and anti-inflammatory activities, which further alleviate the liver fibrosis. Abbreviations BDL: bile duct ligated group, BDL-Se: bile duct ligated-selenium group, MDA: malondialdehyde, TNF-α: tumour necrosis factor-alpha, TGF-β1: transforming growth factor- beta1, ROS: reactive oxygen species, mRNA: messenger RNA, IL-6: interleukin-6, BW: body weight, AST: aspartate aminotransferase, ALT: alanine aminotransferase, ALP: alkaline phosphatase, TP: total proteins, CCl4: carbon tetrachloride, GPx: glutathione peroxidase enzyme, SOD: superoxide dismutase, IL-1: interleukin-1.

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