scholarly journals Evaluating Whether Radiofrequency Irradiation Attenuated UV-B-Induced Skin Pigmentation by Increasing Melanosomal Autophagy and Decreasing Melanin Synthesis

2021 ◽  
Vol 22 (19) ◽  
pp. 10724
Author(s):  
Hyoung Moon Kim ◽  
Seyeon Oh ◽  
Jin Young Yang ◽  
Hye Jin Sun ◽  
Miran Jang ◽  
...  
Keyword(s):  
Skin Color ◽  
Skin Pigmentation ◽  
Signal Pathways ◽  
Tnf Receptor ◽  
Expression Ratio ◽  
Initiation Factors ◽  
Radiation Induced ◽  
Necrosis Factor ◽  
Masson Staining

Autophagy is involved in the degradation of melanosomes and the determination of skin color. TLR4 and tumor necrosis factor (TNF) signaling upregulates NF-kB expression, which is involved in the upregulation of mTOR. The activation of mTOR by UV-B exposure results in decreased autophagy, whereas radiofrequency (RF) irradiation decreases TLR4 and TNF receptor (TNFR) expression. We evaluated whether RF decreased skin pigmentation by restoring autophagy by decreasing the expression of TLR4 or TNFR/NF-κB/mTOR in the UV-B-irradiated animal model. UV-B radiation induced the expressions of TNFR, TLR, and NF-κB in the skin, which were all decreased by RF irradiation. RF irradiation also decreased phosphorylated mTOR expression and upregulated autophagy initiation factors such as FIP200, ULK1, ULK2, ATG13, and ATG101 in the UV-B-irradiated skin. Beclin 1 expression and the expression ratio of LC3-I to LC3-II were increased by UV-B/RF irradiation. Furthermore, melanin-containing autophagosomes increased with RF irradiation. Fontana-Masson staining showed that the amount of melanin deposition in the skin was decreased by RF irradiation. This study showed that RF irradiation decreased skin pigmentation by restoring melanosomal autophagy, and that the possible signal pathways which modulate autophagy could be TLR4, TNFR, NF-κB, and mTOR.

Leukogram and cortisol parameters in Swiss mice experimentally infected with Angiostrongylus costaricensis

2021 ◽  
Vol 95 ◽  
Author(s):  
E. Benvegnú ◽  
C.C. Hermes ◽  
J.A. Guizzo ◽  
S.M. Soares ◽  
M.M. Costa ◽  
...  
Keyword(s):  
Cytokine Profile ◽  
Control Group ◽  
Necrosis Factor Alpha ◽  
Swiss Mice ◽  
Hypochromic Anaemia ◽  
Third Stage ◽  
Factor Alpha ◽  
Cortisol Levels ◽  
Necrosis Factor

Abstract This study describes changes in haematological parameters, cytokine profile, histopathology and cortisol levels in Swiss mice experimentally infected with Angiostrongylus costaricensis. Twenty-eight Swiss mice were divided into two groups (G1 and G2) of 14 animals each. In each group, eight animals were infected orally with ten third-stage larvae of A. costaricensis and six were used as a control group. The mice of groups G1 and G2 were sacrificed 14 and 24 days after infection, respectively. Samples were collected for histopathological and haematological analyses and determination of the cytokine profile and cortisol levels. Granulomatous reaction, eosinophilic infiltrate and vasculitis in the intestinal tract, pancreas, liver and spleen were observed with varying intensity in infected animals. Our results showed that the mice developed normocytic and hypochromic anaemia, and that the histopathological lesions caused by the experimental infection influenced increases in cortisol, neutrophil and monocyte levels. In addition to this, we detected increased interleukin-6 and tumour necrosis factor alpha levels in the infected animals.

scholarly journals The α and β Subunits of IκB Kinase (IKK) Mediate TRAF2-Dependent IKK Recruitment to Tumor Necrosis Factor (TNF) Receptor 1 in Response to TNF

2001 ◽  
Vol 21 (12) ◽  
pp. 3986-3994 ◽  
Author(s):  
Anne Devin ◽  
Yong Lin ◽  
Shoji Yamaoka ◽  
Zhiwei Li ◽  
Michael Karin ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Leucine Zipper ◽  
Nuclear Translocation ◽  
Ring Finger ◽  
Tnf Receptor ◽  
Death Domain ◽  
Iκb Kinase ◽  
Cytokine Tumor Necrosis Factor ◽  
Necrosis Factor

ABSTRACT The activation of IκB kinase (IKK) is a key step in the nuclear translocation of the transcription factor NF-κB. IKK is a complex composed of three subunits: IKKα, IKKβ, and IKKγ (also called NEMO). In response to the proinflammatory cytokine tumor necrosis factor (TNF), IKK is activated after being recruited to the TNF receptor 1 (TNF-R1) complex via TNF receptor-associated factor 2 (TRAF2). We found that the IKKα and IKKβ catalytic subunits are required for IKK-TRAF2 interaction. This interaction occurs through the leucine zipper motif common to IKKα, IKKβ, and the RING finger domain of TRAF2, and either IKKα or IKKβ alone is sufficient for the recruitment of IKK to TNF-R1. Importantly, IKKγ is not essential for TNF-induced IKK recruitment to TNF-R1, as this occurs efficiently in IKKγ-deficient cells. Using TRAF2−/− cells, we demonstrated that the TNF-induced interaction between IKKγ and the death domain kinase RIP is TRAF2 dependent and that one possible function of this interaction is to stabilize the IKK complex when it interacts with TRAF2.

scholarly journals Membrane lymphotoxin-α2β is a novel tumor necrosis factor (TNF) receptor 2 (TNFR2) agonist

2021 ◽  
Vol 12 (4) ◽  
Author(s):  
Kirstin Kucka ◽  
Isabell Lang ◽  
Tengyu Zhang ◽  
Daniela Siegmund ◽  
Juliane Medler ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Asymmetric Structure ◽  
Tnf Receptor ◽  
Membrane Bound ◽  
Necrosis Factor

AbstractIn the early 1990s, it has been described that LTα and LTβ form LTα2β and LTαβ2 heterotrimers, which bind to TNFR1 and LTβR, respectively. Afterwards, the LTαβ2–LTβR system has been intensively studied while the LTα2β–TNFR1 interaction has been ignored to date, presumably due to the fact that at the time of identification of the LTα2β–TNFR1 interaction one knew already two ligands for TNFR1, namely TNF and LTα. Here, we show that LTα2β interacts not only with TNFR1 but also with TNFR2. We furthermore demonstrate that membrane-bound LTα2β (memLTα2β), despite its asymmetric structure, stimulates TNFR1 and TNFR2 signaling. Not surprising in view of its ability to interact with TNFR2, LTα2β is inhibited by Etanercept, which is approved for the treatment of rheumatoid arthritis and also inhibits TNF and LTα.

Tumor necrosis factor-α inhibitors alleviation of experimentally induced neuropathic pain is associated with modulation of TNF receptor expression

2014 ◽  
Vol 92 (11) ◽  
pp. 1490-1498 ◽  
Author(s):  
Pablo Andrade ◽  
Govert Hoogland ◽  
John S. Del Rosario ◽  
Harry W. Steinbusch ◽  
Veerle Visser-Vandewalle ◽  
...  
Keyword(s):  
Neuropathic Pain ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Receptor Expression ◽  
Tnf Receptor ◽  
Factor Α ◽  
Necrosis Factor ◽  
Experimentally Induced

Tumor necrosis factor receptor-mediated apoptosis in Trichinella spiralis-infected muscle cells

Parasitology ◽  
2005 ◽  
Vol 131 (3) ◽  
pp. 373-381 ◽  
Author(s):  
Z. WU ◽  
I. NAGANO ◽  
T. BOONMARS ◽  
Y. TAKAHASHI
Keyword(s):  
Caspase 3 ◽  
Trichinella Spiralis ◽  
Cell Formation ◽  
Muscle Cells ◽  
Cyst Formation ◽  
Signalling Pathway ◽  
Tnf Receptor ◽  
Tnf Α ◽  
Infected Muscle ◽  
Necrosis Factor

In order to reveal the mechanisms underlying nurse cell formation during Trichinella spiralis infection, the expression of the factors of tumor necrosis factor-alpha (TNF-α)/TNF receptor 1 (TNFR-1) signalling pathway mediating apoptosis was investigated. The analysed factors included TNF-α, TNFR-1, TNF receptor-associated death-domain (TRADD), caspase 3, caspase 8, TNF receptor associated factor-2 (TRAF2) and receptor interactive protein (RIP), all of which are involved in the TNF-α/TNFR-1 signalling pathway-mediated apoptosis. The quantitative RT-PCR indicated that the infected muscle tissues up-regulate the expression of pro-apoptosis genes (TNF-α, TNFR-1 and TRADD, caspase 3 and caspase 8), and anti-apoptosis genes (TRAF2 and RIP) at the beginning of cyst formation. The expression returned to the normal level after cyst formation. The quantitative RT-PCR analysis of mRNA from tissue samples isolated by laser capture micro-dissection confirmed that the up-regulation of these genes was restricted in infected muscle cells, was not in the inflammation cells around infected muscle cells nor in normal muscle cells. The in situ localization study of pro-apoptosis (TRADD, caspase 3) and anti-apoptosis gene products (TRAF2) indicated that these were expressed in the basophilic cytoplasm (infected muscle cell origin) of the nurse cells. Thus the present study suggests that the TNF-α/TNFR-1 signalling pathway is involved in nurse cell formation.

scholarly journals Neutralization of Tumor Necrosis Factor (TNF) by Antibody but not TNF Receptor Fusion Molecule Exacerbates Chronic Murine Tuberculosis

2007 ◽  
Vol 195 (11) ◽  
pp. 1643-1650 ◽  
Author(s):  
Hillarie L. Plessner ◽  
P. Ling Lin ◽  
Tadahiko Kohno ◽  
James S. Louie ◽  
Denise Kirschner ◽  
...  
Keyword(s):  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tnf Receptor ◽  
Necrosis Factor
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