scholarly journals Regulation of ultraviolet radiation induced cutaneous photoimmunosuppression by Toll-like receptor-4

2011 ◽  
Vol 508 (2) ◽  
pp. 171-177 ◽  
Author(s):  
Wesley Lewis ◽  
Eva Simanyi ◽  
Hui Li ◽  
Camilla A. Thompson ◽  
Tahseen H. Nasti ◽  
...  
Keyword(s):  
Ultraviolet Radiation ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Radiation Induced

Abstract 525: Toll-like receptor-4 mediated cutaneous immune responses augment ultraviolet radiation-induced DNA damage and tumor development

2012 ◽  
Author(s):  
Israr Ahmad ◽  
Purushotham Guroji ◽  
Hugo Jimenez ◽  
Eva Simanyi ◽  
Anusuiya Nagar ◽  
...  
Keyword(s):  
Dna Damage ◽  
Immune Responses ◽  
Ultraviolet Radiation ◽  
Tumor Development ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Radiation Induced

Toll‐like receptor‐4 deficiency inhibits ultraviolet radiation‐induced tumor development by modulation of immune and inflammatory responses

2020 ◽  
Vol 60 (1) ◽  
pp. 60-70
Author(s):  
Israr Ahmad ◽  
Tahseen H. Nasti ◽  
Heba M. Rihan ◽  
Hugo Jimenez ◽  
Craig A. Elmets ◽  
...  
Keyword(s):  
Ultraviolet Radiation ◽  
Inflammatory Responses ◽  
Tumor Development ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Radiation Induced

scholarly journals 513 The toll like receptor-4 antagonist, TAK-242, enhances repair of ultraviolet radiation-induced DNA damage and inhibits UVB-induced tumor development in mice

2021 ◽  
Vol 141 (5) ◽  
pp. S89
Author(s):  
M.A. Sherwani ◽  
A.S. Abdelgawad ◽  
M. Eraslan ◽  
M. Chung ◽  
C. Elmets ◽  
...  
Keyword(s):  
Dna Damage ◽  
Ultraviolet Radiation ◽  
Tumor Development ◽  
Toll Like Receptor ◽  
Toll Like Receptor 4 ◽  
Radiation Induced

scholarly journals Apoptosis Resistance in Fibroblasts Precedes Progressive Scarring in Pulmonary Fibrosis and Is Partially Mediated by Toll-Like Receptor 4 Activation

2019 ◽  
Vol 170 (2) ◽  
pp. 489-498 ◽  
Author(s):  
Kelly M Hanson ◽  
Eric B Hernady ◽  
Christina K Reed ◽  
Carl J Johnston ◽  
Angela M Groves ◽  
...  
Keyword(s):  
Pulmonary Fibrosis ◽  
Lung Fibroblasts ◽  
Radiation Response ◽  
Mouse Lung ◽  
Environmental Toxicants ◽  
Toll Like Receptor ◽  
Apoptosis Resistance ◽  
Toll Like Receptor 4 ◽  
Increased Risk ◽  
Radiation Induced

Abstract Inhalation of environmental toxicants such as cigarette smoke, metal or wood dust, silica, or asbestos is associated with increased risk for idiopathic pulmonary fibrosis (IPF). IPF involves progressive scarring of lung tissue, which interferes with normal respiration and is ultimately fatal; however, the complex cellular mechanisms of IPF pathogenesis remain unclear. Fibroblast apoptosis is essential in normal wound healing but is dysregulated in IPF. Recent studies suggest that Toll-like receptor 4 (TLR4) is key in the onset of IPF. Here, radiation-induced PF was used as a model for IPF because it very closely mimics the progressive and intractable nature of IPF. Female C57BL/6J (C57) and C57BL/6J TLR4−/− mice were exposed to a single dose of 13 Gy whole-thorax ionizing radiation. Although both strains showed similar levels of immediate radiation-induced damage, C57 mice exhibited more extensive fibrosis at 22-week postirradiation (PI) than TLR4−/− mice. Isolated C57 primary 1° MLFs showed decreased apoptosis susceptibility as early as 8-week postirradiation, a phenotype that persisted for the remainder of the radiation response. TLR4−/− 1° mouse lung fibroblasts did not exhibit significant apoptosis resistance at any point. Systemic release of high mobility group box 1, a TLR4 agonist, during the pneumonitis phase of the radiation response may act through TLR4 to contribute to fibroblast apoptosis resistance and thus interfere with wound resolution. These findings demonstrate that apoptosis resistance occurs earlier in pulmonary fibrosis pathogenesis than previously assumed, and that TLR4 signaling is a key mediator in this process.

660 Deficiency of Toll-like receptor 4 leads to cardioprotection against doxorubicin-induced cardiomyopathy

2007 ◽  
Vol 6 (1) ◽  
pp. 142-143
Author(s):  
A RIAD ◽  
S BIEN ◽  
M GRATZ ◽  
S BERESWILL ◽  
H SCHULTHEISS ◽  
...  
Keyword(s):  
Toll Like Receptor ◽  
Toll Like Receptor 4

Tanshinone IIA attenuates elastase-induced AAA in rats via inhibition of MyD88-dependent TLR-4 signaling

VASA ◽  
2014 ◽  
Vol 43 (1) ◽  
pp. 39-46 ◽  
Author(s):  
Tao Shang ◽  
Feng Ran ◽  
Qian Qiao ◽  
Zhao Liu ◽  
Chang-Jian Liu
Keyword(s):  
Nuclear Factor Κb ◽  
Tanshinone Iia ◽  
Myeloid Differentiation ◽  
Aortic Tissue ◽  
Toll Like Receptor ◽  
Sprague Dawley ◽  
Toll Like Receptor 4 ◽  
Tissue Samples ◽  
Myeloid Differentiation Factor ◽  
And Control

Background: The purpose of this study was to determine whether myeloid differentiation factor88-dependent Toll-Like Receptor-4 (TLR-4) signaling contributed to the inhibition of abdominal aortic aneurysm (AAA) by Tanshinone IIA (Tan IIA). Materials and methods: Male Sprague-Dawley rats (n = 12 / group) were randomly distributed into three groups: Tan IIA, control, and sham. The rats from Tan IIA and control groups under-went intra-aortic elastase perfusion to induce AAAs, and those in the sham group were perfused with saline. Only the Tan IIA group received Tan IIA (2 mg / rat / d). Aortic tissue samples were harvested at 24 d after perfusion and evaluated using reverse transcriptase-polymerase chain reaction, Western blot, immunohistochemistry and immunofluorescence. Results: The over-expression of Toll-Like Receptor-4 (TLR-4), Myeloid Differentiation factor 88 (MyD88), Phosphorylated Nuclear Factor κB (pNF-κB) and Phosphorylated IκBα (pIκBα) induced by elastase perfusion were significantly decreased by Tan IIA treatment. Conclusions: Tan IIA attenuates elastase-induced AAA in rats possibly via the inhibition of MyD88-dependent TLR-4 signaling, which may be one potential explanation of why Tan IIA inhibits AAA development through multiple effects.

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